PL EN


Preferences help
enabled [disable] Abstract
Number of results
2011 | 38 | suplement 1 | 5-124
Article title

Znaczenie wybranych populacji komórek immunologicznych w leczeniu zaostrzeń stwardnienia rozsianego z zastosowaniem plazmaferezy

Content
Title variants
EN
The role of selected immune cell populations in plasma exchange treatment of multiple sclerosis relapses
Languages of publication
PL
Abstracts
EN
Introduction: Multiple sclerosis (MS) is a chronic demyelinating disorder of the central nervous system. In the majority of patients the disease is characterized, at least in the early phase, by relapsing-remitting clinical course. The standard therapy of MS relapse consist of high dose intravenous glucocorticoid treatment. However, in a small group of MS patients this therapy brings no clinical improvement. Numerous studies showed that plasma exchange is an effective therapeutic option for patients with glucocorticoidresistant MS relapse. Elimination of multiple humoral factors has been postulated as a possible therapeutic mechanism of plasma exchange. However, the influence of plasma exchange on cellular immunity remains poorly understood. Aim of the study: The aim of this study was to assess the involvement of cellular immunity in clinical efficacy of plasma exchange as therapy for multiple sclerosis patients suffering from relapses resistant to glucocorticoid pulse therapy. The analysis encompassed main T cell populations (including regulatory T cells), NK cells, NKT cells, B cells and the most important for immunoregulatory processes monocyte and dendritic cell subpopulations. Materials and methods: Peripheral blood was obtained from MS patients suffering from glucocorticoid-resistant relapses at three consecutive time-points of plasma exchange treatment: before the first plasma exchange, after the third plasma exchange and after completion of plasma exchange therapy. Patients with MS relapse with good response to glucocorticoid pulse therapy and healthy individuals served as controls. Peripheral blood mononuclear cells were obtained and immune cell subsets were investigated by flow cytometry ex vivo. In further experiments, the pure monocyte population was isolated from peripheral blood by magnetic sorting. Isolated monocytes were cultured 48 hours under inflammatory conditions. After completion of culture period, surface expression profile of monocytes in vitro, including various co-stimulatory and MHC class II molecules, was assessed by flow cytometry. The secretion of pro-inflammatory and regulatory cytokines by peripheral blood mononuclear cells and monocytes in vitro was analyzed in culture supernatants. Results: The percentage of monocytes expressing CD16 decreased significantly over the course of PE treatment. The effect was specific for the CD14highCD16+ monocyte subpopulation, whereas the CD14lowCD16+ and the “classical” CD14highCD16- subpopulations showed no differences during the treatment. Plasma exchange did not influence the main lymphocyte populations (including regulatory T cells, NK or NKT cells, B cells) and dendritic cell subtypes. A baseline increase in the percentage of CD14highCD16+ monocytes was predictive for a good therapeutic response to plasma exchange treatment. In contrast, PE non-responders were characterized at baseline by lower expression of HLA-DR in CD14highCD16- monocytes. This parameter normalized after completion of plasma exchange, paralleled by increased TNF-α secretion by monocytes in culture. The secretion profile of peripheral blood mononuclear cells was not influenced by plasma exchange therapy. Conclusions: Results obtained in the study demonstrate a significant influence of plasma exchange on the structure and function of immune cells in peripheral blood of patients with glucocorticoid-resistant MS relapse. The diversity of immune effects of plasma exchange depending on the clinical response to therapy suggests complex and inhomogeneous mechanisms of glucocorticoid resistance in MS. These observations may be of particular importance for understanding of clinical effectiveness of plasma exchange in MS relapse as well as for the problem of glucocorticoid sensitivity in inflammatory disorders.
PL
Wstęp: Stwardnienie rozsiane (łac. sclerosis multiplex - SM) jest przewlekłym demielinizacyjnym schorzeniem ośrodkowego układu nerwowego. U większości pacjentów, przynajmniej w początkowym okresie, choroba przebiega pod postacią zaostrzeń (tzw. rzutów) i remisji objawów neurologicznych. Standardem leczenia w rzucie SM jest dożylne podawanie wysokich dawek glukokortykosteroidów. Jednakże, w niewielkiej grupie pacjentów terapia ta nie przynosi pożądanych efektów klinicznych. Liczne badania wykazały, iż plazmafereza stanowi efektywną opcję terapeutyczną dla pacjentów z opornymi na glukokortykosteroidy rzutami SM. Powszechnie uważa się, że skuteczność kliniczna plazmaferezy jest wynikiem usuwania z krwi obwodowej szeregu zróżnicowanych cząsteczek czynnych immunologicznie. Niewiele wiadomo jednak, na temat wpływu plazmaferezy na komórkowe składniki układu immunologicznego. Cel pracy: Celem pracy była ocena zaangażowania komórkowych elementów układu immunologicznego w mechanizmy warunkujące skuteczność kliniczną plazmaferezy w zaostrzeniach stwardnienia rozsianego opornych na terapię glukokortykosteroidami. Badaniem zostały objęte podstawowe populacje limfocytów T (w tym limfocyty T regulatorowe), komórki NK, komórki NKT, limfocyty B oraz najważniejsze z punktu widzenia immunoregulacji subpopulacje monocytów i komórek dendrytycznych krwi obwodowej. Materiały i metody: Krew obwodowa została pobrana od pacjentów z opornym na leczenie glukokortykosteroidami rzutem SM w trzech punktach czasowych terapii plazmaferezą: przed pierwszym zabiegiem plazmaferezy, po trzecim zabiegu plazmaferezy oraz po zakończeniu cyklu plazmaferez. Pacjenci z rzutem SM wrażliwym na terapię glukokortykosteroidami oraz zdrowi ochotnicy stanowili grupy kontrolne. Populacje komórek immunologicznych analizowane były we frakcji komórek jednojądrzastych krwi obwodowej za pomocą cytometrii przepływowej ex vivo. W kolejnej części badania, czysta frakcja monocytów izolowana była z krwi obwodowej z zastosowaniem metody sortowania magnetycznego. Uzyskane w ten sposób monocyty były poddawane 48-godzinnej hodowli w warunkach stymulacji prozapalnej. Po zakończeniu hodowli, profil ekspresji powierzchniowej monocytów in vitro, obejmujący szereg molekuł kostymulacyjnych oraz cząsteczki MHC klasy II, oceniany był metodą cytometrii przepływowej. W dalszych eksperymentach produkcja cytokin prozapalnych i regulacyjnych przez komórki jednojądrzaste oraz monocyty krwi obwodowej in vitro analizowana była w nadsączach hodowlanych. Wyniki: W przebiegu terapii plazmaferezą obserwowano, równolegle do poprawy klinicznej, istotne zmniejszenie frakcji monocytów krwi obwodowej wykazujących ekspresję CD16 ex vivo. Analiza poszczególnych subpopulacji monocytów wykazała, że efekt ten był specyficzny dla subpopulacji CD14highCD16+, podczas gdy subpopulacja monocytów CD14lowCD16+ oraz frakcja „klasycznych” monocytów CD14highCD16- nie wykazywały zmian w trakcie terapii. Terapia plazmaferezą nie miała wpływu na główne populacje limfocytów (m.in. limfocyty T regulatorowe, komórki NK, komórki NKT, limfocyty B) oraz na mieloidalne i plazmacytoidalne komórki dendrytyczne krwi obwodowej. Obserwowane przed rozpoczęciem terapii zwiększenie frakcji monocytów CD14highCD16+ było czynnikiem prognostycznym dobrej odpowiedzi terapeutycznej na plazmaferezę. Natomiast, u pacjentów z negatywną odpowiedzią terapeutyczną obserwowano początkowo zmniejszoną ekspresję HLA-DR w subpopulacji „klasycznych” monocytów CD14highCD16-. Parametr ten ulegał normalizacji po zakończeniu cyklu plazmaferez, czemu towarzyszyła zwiększona sekrecja TNF-α przez monocyty in vitro. W badaniu nie wykazano wpływu terapii plazmaferezą na profil sekrecji całkowitej frakcji komórek jednojądrzastych krwi obwodowej. Wnioski: Uzyskane wyniki dowodzą istotnego wpływu plazmaferezy na strukturę i funkcję komórek krwi obwodowej pacjentów z opornym na glukokortykosteroidy zaostrzeniem SM. Zróżnicowanie efektów immunologicznych plazmaferezy w zależności od odpowiedzi klinicznej na terapię sugeruje istnienie w SM złożonych i niejednorodnych mechanizmów zaburzeń wrażliwości na glukokortykosteroidy. Poczynione w badaniu obserwacje mogą przyczynić się do lepszego zrozumienia efektów klinicznych plazmaferezy w terapii rzutów SM, jak również znaleźć zastosowanie w badaniach nad zagadnieniem oporności na glukokortykosteroidy w chorobach zapalnych.
Discipline
Publisher

Year
Volume
38
Issue
Pages
5-124
Physical description
Contributors
  • Klinika Endokrynologii i Chorób Metabolicznych, Instytut Centrum Zdrowia Matki Polki, mstasiolek@yahoo.de
References
  • Selmaj K. Stwardnienie rozsiane. Termedia Wydawnictwo Medyczne, Poznań 2006.
  • Probert L, Selmaj K. TNF and related molecules: trends in neuroscience and clinical applications. J Neuroimmunol. 1997; 72:113-117.
  • Hohlfeld R, Londei M, Massacesi L, Salvetti M. T-cell autoimmunity in multiple sclerosis. Immunol Today. 1995; 16:259-261.
  • Hafler DA, Weiner HL. Immunologic mechanisms and therapy in multiple sclerosis. Immunol Rev. 1995; 144:75-107.
  • Raine CS. The Norton Lecture: A review of the oligodendrocyte in the multiple sclerosis lesion. J Neuroimmunol. 1997; 77:135-152.
  • Lucchinetti C, Brück W, Parisi J, Scheithauer B, Rodriguez M, Lassmann H. Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination. Ann Neurol. 2000; 47:707-717.
  • Bramow S, Frischer JM, Lassmann H, Koch-Henriksen N, Lucchinetti CF, Sørensen PS i wsp. Demyelination versus remyelination in progressive multiple sclerosis. Brain. 2010; 133:2983-2998.
  • Bjartmar C, Kidd G, Mörk S, Rudick R, Trapp BD. Neurological disability correlates with spinal cord axonal loss and reduced N-acetyl aspartate in chronic multiple sclerosis patients. Ann Neurol. 2000; 48:893-901.
  • Schirmer L, Antel JP, Brück W, Stadelmann C. Axonal Loss and Neurofilament Phosphorylation Changes Accompany Lesion Development and Clinical Progression in Multiple Sclerosis. Brain Pathol. 2010; doi: 10.1111/j.1750-3639.2010.00466.x.
  • DeLuca GC, Williams K, Evangelou N, Ebers GC, Esiri MM. The contribution of demyelination to axonal loss in multiple sclerosis. Brain. 2006; 129:1507-1516.
  • Frischer JM, Bramow S, Dal-Bianco A, Lucchinetti CF, Rauschka H, Schmidbauer M I wsp. The relation between inflammation and neurodegeneration in multiple sclerosis brains. Brain. 2009; 132:1175-1189.
  • Gunnarsson M, Malmeström C, Axelsson M, Sundström P, Dahle C, Vrethem M i wsp. Axonal damage in relapsing multiple sclerosis is markedly reduced by natalizumab. Ann Neurol. 2011; 69:83-89.
  • Raine CS, McFarland HF, Tourtellotte WW. Multiple Sclerosis. Clinical and pathological basis. London: Chapman & Hall, 1997.
  • Brinkman CJ, Nillesen WM, Hommes OR, Lamers KJ, de Pauw BE, Delmotte P. Cell-mediated immunity in multiple sclerosis as determined by sensitivity of different lymphocyte populations to various brain tissue antigens. Ann Neurol. 1982; 11:450-455.
  • Hafler DA, Benjamin DS, Burks J, Weiner HL. Myelin basic protein and proteolipid protein reactivity of brain- and cerebrospinal fluid-derived T cell clones in multiple sclerosis and postinfectious encephalomyelitis. J Immunol. 1987; 139:68-72.
  • Bernard CC, Johns TG, Slavin A, Ichikawa M, Ewing C, Liu J i wsp. Myelin oligodendrocyte glycoprotein: a novel candidate autoantigen in multiple sclerosis. J Mol Med. 1997; 75:77-88.
  • Quarles RH. Myelin-associated glycoprotein in development and disease. Dev Neurosci. 1983-1984; 6:285-303.
  • van Noort JM, van Sechel AC, Bajramovic JJ, el Ouagmiri M, Polman CH, Lassmann H i wsp. The small heat-shock protein alpha B-crystallin as candidate autoantigen in multiple sclerosis. Nature. 1995; 375:798-801.
  • Wekerle H. Experimental autoimmune encephalomyelitis as a model of immune-mediated CNS disease. Curr Opin Neurobiol. 1993; 3:779-784.
  • Peruga I, Hartwig S, Thöne J, Hovemann B, Gold R, Juckel G i wsp. Inflammation modulates anxiety in an animal model of multiple sclerosis. Behav Brain Res. 2011; 220:20-29.
  • Mokhtarian F, McFarlin DE, Raine CS. Adoptive transfer of myelin basic protein-sensitized T cells produces chronic relapsing demyelinating disease in mice. Nature. 1984; 309:356-358.
  • Wujek JR, Bjartmar C, Richer E, Ransohoff RM, Yu M, Tuohy VK i wsp. Axon loss in the spinal cord determines permanent neurological disability in an animal model of multiple sclerosis. J Neuropathol Exp Neurol. 2002; 61:23-32.
  • Owens T, Wekerle H, Antel S. Genetic models for CNS inflammation. Nature Med. 2001; 7:161-166.
  • Das MP, Nicholson LB, Greer JM, Kuchroo VK. Autopathogenic T helper cell type 1 (Th1] and protective Th2 clones differ in their recognition of the autoantigenic peptide of myelin proteolipid protein. J Exp Med. 1997; 186:867-876.
  • Falcone M, Bloom BR. A T helper cell 2 (Th2] immune response against non-self antigens modifies the cytokine profile of autoimmune T cells and protects against experimental allergic encephalomyelitis. J Exp Med. 1997; 185:901-907.
  • Wildbaum G, Youssef S, Grabie N, Karin N. Neutralizing antibodies to IFN-gamma-inducing factor prevent experimental autoimmune encephalomyelitis. J Immunol. 1998; 161:6368-6374.
  • Kuchroo VK, Anderson AC, Waldner H, Munder M, Bettelli E, Nicholson LB. T cell response in experimental autoimmune encephalomyelitis (EAE): role of self and cross-reactive antigens in shaping, tuning, and regulating the autopathogenic T cell repertoire. Annu Rev Immunol. 2002; 20:101-123.
  • Mosmann TR, Sad S. The expanding universe of T-cell subsets: Th1, Th2 and more. Immunol Today. 1996; 17:138-146.
  • Nicholson LB, Kuchroo VK. Manipulation of the Th1/Th2 balance in autoimmune disease. Curr Opin Immunol. 1996; 8:837-842.
  • Aggarwal S, Ghilardi N, Xie MH, de Sauvage FJ, Gurney AL. Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17. J Biol Chem. 2003; 278:1910-1914.
  • Hofstetter HH, Ibrahim SM, Koczan D, Kruse N, Weishaupt A, Toyka K i wsp. Therapeutic efficacy of IL-17 neutralization in murine experimental autoimmune encephalomyelitis. Cell Immunol. 2005; 237:123-130.
  • Komiyama Y, Nakae S, Matsuki T, Nambu A, Ishigame H, Kakuta S i wsp. IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis. J Immunol. 2006; 177:566-573.
  • Gocke AR, Cravens PD, Ben LH, Hussain RZ, Northrop SC, Racke MK i wsp. T-bet regulates the fate of Th1 and Th17 lymphocytes in autoimmunity. J Immunol. 2007; 178:1341-1348.
  • O'Connor RA, Prendergast CT, Sabatos CA, Lau CW, Leech MD, Wraith DC i wsp. Th1 cells facilitate the entry of Th17 cells to the central nervous system during experimental autoimmune encephalomyelitis. J Immunol. 2008; 181:3750-3754.
  • Frisullo G, Nociti V, Iorio R, Patanella AK, Marti A, Caggiula M i wsp. IL17 and IFNgamma production by peripheral blood mononuclear cells from clinically isolated syndrome to secondary progressive multiple sclerosis. Cytokine. 2008; 44:22-25.
  • Kebir H, Ifergan I, Alvarez JI, Bernard M, Poirier J, Arbour N i wsp. Preferential recruitment of interferon-gamma-expressing TH17 cells in multiple sclerosis. Ann Neurol. 2009; 66:390-402.
  • Axtell RC, de Jong BA, Boniface K, van der Voort LF, Bhat R, De Sarno P i wsp. T helper type 1 and 17 cells determine efficacy of interferon-beta in multiple sclerosis and experimental encephalomyelitis. Nat Med. 2010; 16:406-412.
  • Berer K, Wekerle H, Krishnamoorthy G. B cells in spontaneous autoimmune diseases of the central nervous system. Mol Immunol. 2010; doi:10.1016/j.molimm.2010.10.025
  • Walsh MJ, Tourtellotte WW, Roman J, Dreyer W. Immunoglobulin G, A, and M--clonal restriction in multiple sclerosis cerebrospinal fluid and serum--analysis by two-dimensional electrophoresis. Clin Immunol Immunopathol. 1985; 35:313-327.
  • Baranzini SE, Jeong MC, Butunoi C, Murray RS, Bernard CC, Oksenberg JR. B cell repertoire diversity and clonal expansion in multiple sclerosis brain lesions. J Immunol. 1999; 163:5133-5144.
  • Berger T, Rubner P, Schautzer F, Egg R, Ulmer H, Mayringer I i wsp. Antimyelin antibodies as a predictor of clinically definite multiple sclerosis after a first demyelinating event. N Engl J Med. 2003; 349:139-145.
  • Martin R, McFarland HF, McFarlin DE. Immunological aspects of demyelinating diseases. Annu Rev Immunol. 1992; 10:153-187.
  • Stasiolek M, Bayas A, Kruse N, Wieczarkowiecz A, Toyka KV, Gold R i wsp. Impaired maturation and altered regulatory function of plasmacytoid dendritic cells in multiple sclerosis. Brain. 2006; 129:1293-1305.
  • Bayas A, Stasiolek M, Kruse N, Toyka KV, Selmaj K, Gold R. Altered innate immune response of plasmacytoid dendritic cells in multiple sclerosis. Clin Exp Immunol. 2009; 157:332-342.
  • Stasiolek M. The role of selected immunoregulatory cell populations in the autoimmune demeylination. Neuro Endocrinol Lett. 2011; 32:101-109
  • Lünemann A, Tackenberg B, Deangelis T, Barreira da Silva R, Messmer B, Vanoaica LD i wsp. Impaired IFN-{gamma} production and proliferation of NK cells in Multiple Sclerosis. Int Immunol. 2011; 23:139-148.
  • O'Keeffe J, Gately CM, Counihan T, Hennessy M, Leahy T, Moran AP i wsp. T-cells expressing natural killer (NK) receptors are altered in multiple sclerosis and responses to alpha-galactosylceramide are impaired. J Neurol Sci. 2008; 275:22-28.
  • Gandhi R, Laroni A, Weiner HL. Role of the innate immune system in the pathogenesis of multiple sclerosis. J Neuroimmunol. 2010; 221:7-14.
  • Burger DR, Ford D, Vetto RM, Hamblin A, Goldstein A, Hubbard M i wsp. Endothelial cell presentation of antigen to human T cells. Hum Immunol. 1981; 3:209-230.
  • Geppert TD, Lipsky PE. Antigen presentation by interferon-gamma-treated endothelial cells and fibroblasts: differential ability to function as antigen-presenting cells despite comparable Ia expression. J Immunol. 1985; 135:3750-3762.
  • Fierz W, Endler B, Reske K, Wekerle H, Fontana A. Astrocytes as antigen-presenting cells. I. Induction of Ia antigen expression on astrocytes by T cells via immune interferon and its effect on antigen presentation. J Immunol. 1985; 134:3785-3793.
  • Banchereau J, Steinman RM. Dendritic cells and the control of immunity. Nature. 1998; 392:245-252.
  • Shortman K, Liu YJ. Mouse and human dendritic cell subtypes. Nat Rev Immunol. 2002; 2:151-161.
  • Adema GJ, Hartgers F, Verstraten R, de Vries E, Marland G, Menon S i wsp. A dendritic-cell-derived C-C chemokine that preferentially attracts naive T cells. Nature. 1997; 387:713-717.
  • Croft M, Duncan DD, Swain SL. Response of naive antigen-specific CD4+ T cells in vitro: characteristics and antigen-presenting cell requirements. J Exp Med. 1992; 176:1431-1437.
  • Brossart P, Bevan MJ. Presentation of exogenous protein antigens on major histocompatibility complex class I molecules by dendritic cells: pathway of presentation and regulation by cytokines. Blood. 1997; 90:1594-1599.
  • Volkmann A, Zal T, Stockinger B. Antigen-presenting cells in the thymus that can negatively select MHC class II-restricted T cells recognizing a circulating self antigen. J Immunol. 1997; 158:693-706.
  • Oppmann B, Lesley R, Blom B, Timans JC, Xu Y, Hunte B i wsp. Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. Immunity. 2000; 13:715-725.
  • Agrawal S, Gupta S, Agrawal A. Human dendritic cells activated via dectin-1 are efficient at priming Th17, cytotoxic CD8 T and B cell responses. PLoS One. 2010; 5:e13418.
  • Rissoan MC, Soumelis V, Kadowaki N, Grouard G, Briere F, de Waal Malefyt R i wsp. Reciprocal control of T helper cell and dendritic cell differentiation. Science. 1999; 283:1183-1186.
  • Moseman EA, Liang X, Dawson AJ, Panoskaltsis-Mortari A, Krieg AM, Liu YJ i wsp. Human plasmacytoid dendritic cells activated by CpG Oligodeo-xynucleotides induce the generation of CD4+CD25+ regulatory T cells. J Immunol. 2004; 173:4433-4442.
  • Ito T, Yang M, Wang YH, Lande R, Gregorio J, Perng OA i wsp. Plasmacytoid dendritic cells prime IL-10-producing T regulatory cells by inducible costimulator ligand. J Exp Med. 2007; 204:105-115.
  • Dzionek A, Fuchs A, Schmidt P, Cremer S, Zysk M, Miltenyi S i wsp. BDCA-2, BDCA-3, and BDCA-4: three markers for distinct subsets of dendritic cells in human peripheral blood. J Immunol. 2000; 165:6037-6046.
  • Dittel BN, Visintin I, Merchant RM, Janeway CA Jr. Presentation of the self antigen myelin basic protein by dendritic cells leads to experimental autoimmune encephalomyelitis. J Immunol. 1999; 163:32-39.
  • Weir CR, Nicolson K, Bäckström BT. Experimental autoimmune encephalomyelitis induction in naive mice by dendritic cells presenting a self-peptide. Immunol Cell Biol. 2002; 80:14-20.
  • Serafini B, Columba-Cabezas S, Di Rosa F, Aloisi F. Intracerebral recruitment and maturation of dendritic cells in the onset and progression of experimental autoimmune encephalomyelitis. Am J Pathol. 2000; 157:1991-2002.
  • Huang YM, Yang JS, Xu LY, Link H, Xiao BG. Autoantigen-pulsed dendritic cells induce tolerance to experimental allergic encephalomyelitis (EAE) in Lewis rats. Clin Exp Immunol. 2000; 122:437-444.
  • Menges M, Rössner S, Voigtländer C, Schindler H, Kukutsch NA, Bogdan C i wsp. Repetitive injections of dendritic cells matured with tumor necrosis factor alpha induce antigen-specific protection of mice from autoimmunity. J Exp Med. 2002; 195:15-21.
  • Bailey SL, Schreiner B, McMahon EJ, Miller SD. CNS myeloid DCs presenting endogenous myelin peptides 'preferentially' polarize CD4+ T(H)-17 cells in relapsing EAE. Nat Immunol. 2007; 8:172-180.
  • Bailey-Bucktrout SL, Caulkins SC, Goings G, Fischer JA, Dzionek A, Miller SD. Cutting edge: central nervous system plasmacytoid dendritic cells regulate the severity of relapsing experimental autoimmune encephalomyelitis. J Immunol. 2008; 180:6457-6461.
  • Schwab N, Zozulya AL, Kieseier BC, Toyka KV, Wiendl H. An imbalance of two functionally and phenotypically different subsets of plasmacytoid dendritic cells characterizes the dysfunctional immune regulation in multiple sclerosis. J Immunol. 2010; 184:5368-5374.
  • López C, Comabella M, Al-zayat H, Tintoré M, Montalban X. Altered maturation of circulating dendritic cells in primary progressive MS patients. J Neuroimmunol. 2006; 175:183-191.
  • Pashenkov M, Huang YM, Kostulas V, Haglund M, Söderström M, Link H. Two subsets of dendritic cells are present in human cerebrospinal fluid. Brain. 2001; 124:480-492.
  • Longhini AL, von Glehn F, Brandão CO, de Paula RF, Pradella F, Moraes AS i wsp. Plasmacytoid dendritic cells are increased in cerebrospinal fluid of untreated patients during multiple sclerosis relapse. J Neuroinflammation. 2011; 8:2.
  • Serafini B, Rosicarelli B, Magliozzi R, Stigliano E, Capello E, Mancardi GL i wsp. Dendritic cells in multiple sclerosis lesions: maturation stage, myelin uptake, and interaction with proliferating T cells. J Neuropathol Exp Neurol. 2006; 65:124-141.
  • Lande R, Gafa V, Serafini B, Giacomini E, Visconti A, Remoli M i wsp. Plasmacytoid dendritic cells in multiple sclerosis: intracerebral recruitment and impaired maturation in response to interferon-beta. J Neuropathol Exp Neurol. 2008; 67:388-401.
  • Navarro J, Aristimuño C, Sánchez-Ramón S, Vigil D, Martínez-Ginés ML, Fernández-Cruz E i wsp. Circulating dendritic cells subsets and regulatory T-cells at multiple sclerosis relapse: differential short-term changes on corticosteroids therapy. J Neuroimmunol. 2006; 176:153-161.
  • Randolph GJ, Jakubzick C, Qu C. Antigen presentation by monocytes and monocyte-derived cells. Curr Opin Immunol. 2008; 20:52-60.
  • Danis VA, Franic GM, Rathjen DA, Brooks PM. Effects of granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-2, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and IL-6 on the production of immunoreactive IL-1 and TNF-alpha by human monocytes. Clin Exp Immunol. 1991; 85:143-150.
  • Hart PH, Whitty GA, Piccoli DS, Hamilton JA. Synergistic activation of human monocytes by granulocyte-macrophage colony-stimulating factor and IFN-gamma. Increased TNF-alpha but not IL-1 activity. J Immunol. 1988; 141:1516-1521.
  • Hart PH, Whitty GA, Piccoli DS, Hamilton JA. Control by IFN-gamma and PGE2 of TNF alpha and IL-1 production by human monocytes. Immunology. 1989; 66:376-383.
  • Bailly S, Ferrua B, Fay M, Gougerot-Pocidalo MA. Differential regulation of IL 6, IL 1 A, IL 1 beta and TNF alpha production in LPS-stimulated human monocytes: role of cyclic AMP.Cytokine. 1990; 2:205-210.
  • Ribbens C, Dayer JM, Chizzolini C. CD40-CD40 ligand (CD154] engagement is required but may not be sufficient for human T helper 1 cell induction of interleukin-2- or interleukin-15-driven, contact-dependent, interleukin-1beta production by monocytes. Immunology. 2000; 99:279-286.
  • Burger D, Dayer JM. The role of human T-lymphocyte-monocyte contact in inflammation and tissue destruction. Arthritis Res. 2002; 4:169-176.
  • Tacke F, Ginhoux F, Jakubzick C, van Rooijen N, Merad M, Randolph GJ. Immature monocytes acquire antigens from other cells in the bone marrow and present them to T cells after maturing in the periphery. J Exp Med. 2006; 203:583-597.
  • Ziegler-Heitbrock L. The CD14+ CD16+ blood monocytes: their role in infection and inflammation. J Leukoc Biol. 2007; 81:584-592.
  • Ziegler-Heitbrock HW, Passlick B, Flieger D. The monoclonal antimonocyte antibody My4 stains B lymphocytes and two distinct monocyte subsets in human peripheral blood. Hybridoma. 1988; 7:521-527.
  • Passlick B, Flieger D, Ziegler-Heitbrock HW. Identification and characterization of a novel monocyte subpopulation in human peripheral blood. Blood. 1989; 74:2527-2534.
  • Ziegler-Heitbrock HW, Fingerle G, Ströbel M, Schraut W, Stelter F, Schütt C i wsp. The novel subset of CD14+/CD16+ blood monocytes exhibits features of tissue macrophages. Eur J Immunol. 1993; 23:2053-2058.
  • Skrzeczyńska-Moncznik J, Bzowska M, Loseke S, Grage-Griebenow E, Zembala M, Pryjma J. Peripheral blood CD14high CD16+ monocytes are main producers of IL-10. Scand J Immunol. 2008; 67:152-159.
  • Kim WK, Sun Y, Do H, Autissier P, Halpern EF, Piatak M Jr i wsp. Monocyte heterogeneity underlying phenotypic changes in monocytes according to SIV disease stage. J Leukoc Biol. 2010; 87:557-567.
  • Landsman L, Varol C, Jung S. Distinct differentiation potential of blood monocyte subsets in the lung. J Immunol. 2007; 178:2000-2007.
  • Randolph GJ, Beaulieu S, Lebecque S, Steinman RM, Muller WA. Differentiation of monocytes into dendritic cells in a model of transendothelial trafficking. Science. 1998; 282:480-483.
  • León B, López-Bravo M, Ardavín C. Monocyte-derived dendritic cells formed at the infection site control the induction of protective T helper 1 responses against Leishmania. Immunity. 2007; 26:519-531.
  • Ifergan I, Kébir H, Bernard M, Wosik K, Dodelet-Devillers A, Cayrol R i wsp. The blood-brain barrier induces differentiation of migrating monocytes into Th17-polarizing dendritic cells. Brain. 2008; 131:785-799.
  • Mildner A, Mack M, Schmidt H, Brück W, Djukic M, Zabel MD i wsp. CCR2+Ly-6Chi monocytes are crucial for the effector phase of autoimmunity in the central nervous system. Brain. 2009; 132:2487-2500.
  • King IL, Dickendesher TL, Segal BM. Circulating Ly-6C+ myeloid precursors migrate to the CNS and play a pathogenic role during autoimmune demyelinating disease. Blood. 2009; 113:3190-3197.
  • Zhu B, Bando Y, Xiao S, Yang K, Anderson AC, Kuchroo VK i wsp. CD11b+Ly-6C(hi) suppressive monocytes in experimental autoimmune encephalomyelitis. J Immunol. 2007; 179:5228-5237.
  • Mikita J, Dubourdieu-Cassagno N, Deloire MS, Vekris A, Biran M, Raffard G i wsp. Altered M1/M2 activation patterns of monocytes in severe relapsing experimental rat model of multiple sclerosis. Amelioration of clinical status by M2 activated monocyte administration. Mult Scler. 2011; 17:2-15.
  • Bahbouhi B, Pettré S, Berthelot L, Garcia A, Elong Ngono A, Degauque N i wsp. T cell recognition of self-antigen presenting cells by protein transfer assay reveals a high frequency of anti-myelin T cells in multiple sclerosis. Brain. 2010; 133:1622-1636.
  • Mitsdoerffer M, Schreiner B, Kieseier BC, Neuhaus O, Dichgans J, Hartung HP i wsp. Monocyte-derived HLA-G acts as a strong inhibitor of autologous CD4 T cell activation and is upregulated by interferon-beta in vitro and in vivo: rationale for the therapy of multiple sclerosis. J Neuroimmunol. 2005; 159:155-164.
  • Jensen MA, Yanowitch RN, Reder AT, White DM, Arnason BG. Immunoglobulin-like transcript 3, an inhibitor of T cell activation, is reduced on blood monocytes during multiple sclerosis relapses and is induced by interferon beta-1b. Mult Scler. 2010; 16:30-38.
  • van Boxel-Dezaire AH, Zula JA, Xu Y, Ransohoff RM, Jacobberger JW, Stark GR. Major differences in the responses of primary human leukocyte subsets to IFN-beta. J Immunol. 2010; 185:5888-5899.
  • Wipfler P, Oppermann K, Pilz G, Afazel S, Haschke-Becher E, Harrer A i wsp. Adhesion molecules are promising candidates to establish surrogate markers for natalizumab treatment. Mult Scler. 2011; 17:16-23.
  • Wiesemann E, Deb M, Trebst C, Hemmer B, Stangel M, Windhagen A. Effects of interferon-beta on co-signaling molecules: upregulation of CD40, CD86 and PD-L2 on monocytes in relation to clinical response to interferon-beta treatment in patients with multiple sclerosis. Mult Scler. 2008; 14:166-176.
  • Burger D, Molnarfi N, Weber MS, Brandt KJ, Benkhoucha M, Gruaz L i wsp. Glatiramer acetate increases IL-1 receptor antagonist but decreases T cell-induced IL-1beta in human monocytes and multiple sclerosis. Proc Natl Acad Sci U S A. 2009; 106:4355-4359.
  • Carpintero R, Brandt KJ, Gruaz L, Molnarfi N, Lalive PH, Burger D. Glatiramer acetate triggers PI3Kδ/Akt and MEK/ERK pathways to induce IL-1 receptor antagonist in human monocytes. Proc Natl Acad Sci U S A. 2010; 107:17692-17697.
  • Comabella M, Lünemann JD, Río J, Sánchez A, López C, Julià E i wsp. A type I interferon signature in monocytes is associated with poor response to interferon-beta in multiple sclerosis. Brain. 2009; 132:3353-3365.
  • Huang YM, Hussien Y, Yarilin D, Xiao BG, Liu YJ, Link H. Interferon-beta induces the development of type 2 dendritic cells. Cytokine. 2001; 13:264-271.
  • Huang YM, Stoyanova N, Jin YP, Teleshova N, Hussien Y, Xiao BG i wsp. Altered phenotype and function of blood dendritic cells in multiple sclerosis are modulated by IFN-beta and IL-10. Clin Exp Immunol. 2001; 124:306-314.
  • Hussien Y, Sanna A, Söderström M, Link H, Huang YM. Glatiramer acetate and IFN-beta act on dendritic cells in multiple sclerosis. J Neuroimmunol. 2001; 121:102-110.
  • Berghella AM, Totaro R, Pellegrini P, Contasta I, Russo T, Carolei A i wsp. Immunological study of IFNbeta-1a-treated and untreated multiple sclerosis patients: clarifying IFNbeta mechanisms and establishing specific dendritic cell immunotherapy. Neuroimmunomodulation. 2005; 12:29-44.
  • Bartosik-Psujek H, Tabarkiewicz J, Pocinska K, Stelmasiak Z, Rolinski J. Immunomodulatory effects of vitamin D on monocyte-derived dendritic cells in multiple sclerosis. Mult Scler. 2010; 16:1513-1516.
  • Lechmann M, Kremmer E, Sticht H, Steinkasserer A. Overexpression, purification, and biochemical characterization of the extracellular human CD83 domain and generation of monoclonal antibodies. Protein Expr Purif. 2002; 24:445-452.
  • Zhou LJ, Tedder TF. Human blood dendritic cells selectively express CD83, a member of the immunoglobulin superfamily. J Immunol. 1995; 154:3821-3835.
  • Kozlow EJ, Wilson GL, Fox CH, Kehrl JH. Subtractive cDNA cloning of a novel member of the Ig gene superfamily expressed at high levels in activated B lymphocytes. Blood. 1993; 81:454-461.
  • Aerts-Toegaert C, Heirman C, Tuyaerts S, Corthals J, Aerts JL, Bonehill A i wsp. CD83 expression on dendritic cells and T cells: correlation with effective immune responses. Eur J Immunol. 2007; 37:686-695.
  • Iking-Konert C, Csekö C, Wagner C, Stegmaier S, Andrassy K, Hänsch GM.Transdifferentiation of polymorphonuclear neutrophils: acquisition of CD83 and other functional characteristics of dendritic cells. J Mol Med. 2001; 79:464-474.
  • Hock BD, Kato M, McKenzie JL, Hart DN. A soluble form of CD83 is released from activated dendritic cells and B lymphocytes, and is detectable in normal human sera. Int Immunol. 2001; 13:959-967.
  • Scholler N, Hayden-Ledbetter M, Hellström KE, Hellström I, Ledbetter JA. CD83 is an I-type lectin adhesion receptor that binds monocytes and a subset of activated CD8+ T cells. J Immunol. 2001; 166:3865-3872.
  • Scholler N, Hayden-Ledbetter M, Dahlin A, Hellström I, Hellström KE, Ledbetter JA. Cutting edge: CD83 regulates the development of cellular immunity. J Immunol. 2002; 168:2599-2602.
  • Hirano N, Butler MO, Xia Z, Ansén S, von Bergwelt-Baildon MS, Neuberg D i wsp. Engagement of CD83 ligand induces prolonged expansion of CD8+ T cells and preferential enrichment for antigen specificity. Blood. 2006; 107:1528-1536.
  • Lechmann M, Krooshoop DJ, Dudziak D, Kremmer E, Kuhnt C, Figdor CG i wsp. The extracellular domain of CD83 inhibits dendritic cell-mediated T cell stimulation and binds to a ligand on dendritic cells. J Exp Med. 2001; 194:1813-1821.
  • Fujimoto Y, Tu L, Miller AS, Bock C, Fujimoto M, Doyle C i wsp. CD83 expression influences CD4+ T cell development in the thymus. Cell. 2002; 108:755-767.
  • García-Martínez LF, Appleby MW, Staehling-Hampton K, Andrews DM, Chen Y, McEuen M i wsp. A novel mutation in CD83 results in the development of a unique population of CD4+ T cells. J Immunol. 2004; 173:2995-3001.
  • Allavena P, Badolato R, Facchetti F, Vermi W, Paganin C, Luini W i wsp. Monocytes from Wiskott-Aldrich patients differentiate in functional mature dendritic cells with a defect in CD83 expression. Eur J Immunol. 2001; 31:3413-3421.
  • Henry J, Miller MM, Pontarotti P. Structure and evolution of the extended B7 family. Immunol Today. 1999; 20:285-288.
  • Zeng C, Wu T, Zhen Y, Xia XP, Zhao Y. BTLA, a new inhibitory B7 family receptor with a TNFR family ligand. Cell Mol Immunol. 2005; 2:427-432.
  • Chambers CA. The expanding world of co-stimulation: the two-signal model revisited. Trends Immunol. 2001; 22:217-223.
  • Chambers CA, Allison JP. Costimulatory regulation of T cell function. Curr Opin Cell Biol. 1999; 11:203-210.
  • Brunner MC, Chambers CA, Chan FK, Hanke J, Winoto A, Allison JP. CTLA-4-Mediated inhibition of early events of T cell proliferation. J Immunol. 1999; 162:5813-5820.
  • Oosterwegel MA, Greenwald RJ, Mandelbrot DA, Lorsbach RB, Sharpe AH. CTLA-4 and T cell activation. Curr Opin Immunol. 1999; 11:294-300.
  • Perez VL, Van Parijs L, Biuckians A, Zheng XX, Strom TB, Abbas AK. Induction of peripheral T cell tolerance in vivo requires CTLA-4 engagement. Immunity. 1997; 6:411-417.
  • Gravestein LA, Borst J. Tumor necrosis factor receptor family members in the immune system. Semin Immunol. 1998; 10:423-434.
  • Lane PJ, Brocker T. Developmental regulation of dendritic cell function. Curr Opin Immunol. 1999; 11:308-313.
  • van Kooten C, Banchereau J. Functions of CD40 on B cells, dendritic cells and other cells. Curr Opin Immunol. 1997; 9:330-337.
  • Ma DY, Clark EA. The role of CD40 and CD154/CD40L in dendritic cells. Semin Immunol. 2009; 21:265-272.
  • Bleharski JR, Niazi KR, Sieling PA, Cheng G, Modlin RL. Signaling lymphocytic activation molecule is expressed on CD40 ligand-activated dendritic cells and directly augments production of inflammatory cytokines. J Immunol. 2001; 167:3174-3181.
  • Cella M, Scheidegger D, Palmer-Lehmann K, Lane P, Lanzavecchia A, Alber G. Ligation of CD40 on dendritic cells triggers production of high levels of interleukin-12 and enhances T cell stimulatory capacity: T-T help via APC activation. J Exp Med. 1996; 184:747-752.
  • Frasca L, Scottà C, Lombardi G, Piccolella E. Human anergic CD4+ T cells can act as suppressor cells by affecting autologous dendritic cell conditioning and survival. J Immunol. 2002; 168:1060-1068.
  • Notarangelo LD, Peitsch MC, Abrahamsen TG, Bachelot C, Bordigoni P, Cant AJ i wsp. CD40lbase: a database of CD40L gene mutations causing X-linked hyper-IgM syndrome. Immunol Today. 1996; 17:511-516.
  • Mehling A, Loser K, Varga G, Metze D, Luger TA, Schwarz T i wsp. Overexpression of CD40 ligand in murine epidermis results in chronic skin inflammation and systemic autoimmunity. J Exp Med. 2001; 194:615-628.
  • Levings MK, Roncarolo MG. T-regulatory 1 cells: a novel subset of CD4 T cells with immunoregulatory properties. J Allergy Clin Immunol. 2000; 106:109-112.
  • Chen Y, Kuchroo VK, Inobe J, Hafler DA, Weiner HL. Regulatory T cell clones induced by oral tolerance: suppression of autoimmune encephalomyelitis. Science. 1994; 265:1237-1240.
  • Sun D, Ben-Nun A, Wekerle H. Regulatory circuits in autoimmunity: recruitment of counter-regulatory CD8+ T cells by encephalitogenic CD4+ T line cells. Eur J Immunol. 1988; 18:1993-1999.
  • Curotto de Lafaille MA, Lafaille JJ. Natural and adaptive foxp3+ regulatory T cells: more of the same or a division of labor? Immunity. 2009 May;30[5]:626-35.
  • Jordan MS, Boesteanu A, Reed AJ, Petrone AL, Holenbeck AE, Lerman MA i wsp. Thymic selection of CD4+CD25+ regulatory T cells induced by an agonist self-peptide.Nat Immunol. 2001; 2:301-306.
  • Bayer AL, Yu A, Malek TR. Function of the IL-2R for thymic and peripheral CD4+CD25+ Foxp3+ T regulatory cells.J Immunol. 2007; 178:4062-4071.
  • Malek TR, Yu A, Zhu L, Matsutani T, Adeegbe D, Bayer AL. IL-2 family of cytokines in T regulatory cell development and homeostasis. J Clin Immunol. 2008; 28:635-639.
  • Corthay A. How do regulatory T cells work? Scand J Immunol. 2009; 70:326-336.
  • Sakaguchi S, Ono M, Setoguchi R, Yagi H, Hori S, Fehervari Z i wsp. Foxp3+ CD25+ CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease. Immunol Rev. 2006; 212:8-27.
  • Yamazaki S, Iyoda T, Tarbell K, Olson K, Velinzon K, Inaba K i wsp. Direct expansion of functional CD25+ CD4+ regulatory T cells by antigen-processing dendritic cells. J Exp Med. 2003; 198:235-247.
  • Yamazaki S, Bonito AJ, Spisek R, Dhodapkar M, Inaba K, Steinman RM. Dendritic cells are specialized accessory cells along with TGF- for the differentiation of Foxp3+ CD4+ regulatory T cells from peripheral Foxp3 precursors. Blood. 2007; 110:4293-4302.
  • Thornton AM, Shevach EM. CD4+CD25+ immunoregulatory T cells suppress polyclonal T cell activation in vitro by inhibiting interleukin 2 production. J Exp Med. 1998; 188:287-296.
  • Takahashi T, Kuniyasu Y, Toda M, Sakaguchi N, Itoh M, Iwata M i wsp. Immunologic self-tolerance maintained by CD25+CD4+ naturally anergic and suppressive T cells: induction of autoimmune disease by breaking their anergic/suppressive state. Int Immunol. 1998; 10:1969-1980.
  • Huter EN, Stummvoll GH, DiPaolo RJ, Glass DD, Shevach EM. Cutting edge: antigen-specific TGF beta-induced regulatory T cells suppress Th17-mediated autoimmune disease. J Immunol. 2008; 181:8209-8213.
  • Yu P, Gregg RK, Bell JJ, Ellis JS, Divekar R, Lee HH i wsp. Specific T regulatory cells display broad suppressive functions against experimental allergic encephalomyelitis upon activation with cognate antigen. J Immunol. 2005; 174:6772-6780.
  • Pandolfi F, Cianci R, Pagliari D, Landolfi R, Cammarota G. Cellular mediators of inflammation: tregs and TH17 cells in gastrointestinal diseases. Mediators Inflamm. 2009; 2009:132028.
  • Hsieh CS, Zheng Y, Liang Y, Fontenot JD, Rudensky AY. An intersection between the self-reactive regulatory and nonregulatory T cell receptor repertoires. Nat Immunol. 2006; 7:401-410.
  • Pacholczyk R, Kern J, Singh N, Iwashima M, Kraj P, Ignatowicz L. Nonself-antigens are the cognate specificities of Foxp3+ regulatory T cells. Immunity. 2007; 27:493-504.
  • Stephens GL, Shevach EM. Foxp3+ regulatory T cells: selfishness under scrutiny. Immunity. 2007; 27:417-419.
  • Kullberg MC, Jankovic D, Gorelick PL, Caspar P, Letterio JJ, Cheever AW i wsp. Bacteria-triggered CD4(+) T regulatory cells suppress Helicobacter hepaticus-induced colitis. J Exp Med. 2002; 196:505-515.
  • Aluvihare VR, Kallikourdis M, Betz AG. Regulatory T cells mediate maternal tolerance to the fetus. Nat Immunol. 2004; 5:266-271.
  • Akbari O, Freeman GJ, Meyer EH, Greenfield EA, Chang TT, Sharpe AH i wsp. Antigen-specific regulatory T cells develop via the ICOS-ICOS-ligand pathway and inhibit allergen-induced airway hyperreactivity. Nat Med. 2002; 8:1024-1032.
  • Sakaguchi S, Sakaguchi N, Asano M, Itoh M, Toda M. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases. J Immunol. 1995; 155:1151-1164.
  • Pandolfi F, Pierdominici M, Marziali M, Livia Bernardi M, Antonelli G, Galati V i wsp. Low-dose IL-2 reduces lymphocyte apoptosis and increases naive CD4 cells in HIV-1 patients treated with HAART. Clin Immunol. 2000; 94:153-159.
  • Wing K, Onishi Y, Prieto-Martin P, Yamaguchi T, Miyara M, Fehervari Z i wsp. CTLA-4 control over Foxp3+ regulatory T cell function. Science. 2008; 322:271-275.
  • Liang B, Workman C, Lee J, Chew C, Dale BM, Colonna L i wsp. Regulatory T cells inhibit dendritic cells by lymphocyte activation gene-3 engagement of MHC class II. J Immunol. 2008; 180:5916-5926.
  • Miyara M, Sakaguchi S. Natural regulatory T cells: mechanisms of suppression. Trends Mol Med. 2007; 13:108-116.
  • Grossman WJ, Verbsky JW, Barchet W, Colonna M, Atkinson JP, Ley TJ. Human T regulatory cells can use the perforin pathway to cause autologous target cell death. Immunity. 2004; 21:589-601.
  • Stephens LA, Malpass KH, Anderton SM. Curing CNS autoimmune disease with myelin-reactive Foxp3+ Treg. Eur J Immunol. 2009; 39:1108-1117.
  • Polanczyk MJ, Hopke C, Huan J, Vandenbark AA, Offner H. Enhanced FoxP3 expression and Treg cell function in pregnant and estrogen-treated mice. J Neuroimmunol. 2005; 170:85-92.
  • Chen X, Winkler-Pickett RT, Carbonetti NH, Ortaldo JR, Oppenheim JJ, Howard OM. Pertussis toxin as an adjuvant suppresses the number and function of CD4+CD25+ T regulatory cells. Eur J Immunol. 2006; 36:671-680.
  • Ephrem A, Chamat S, Miquel C, Fisson S, Mouthon L, Caligiuri G i wsp. Expansion of CD4+CD25+ regulatory T cells by intravenous immunoglobulin: a critical factor in controlling experimental autoimmune encephalomyelitis. Blood. 2008; 111:715-722.
  • Platten M, Youssef S, Hur EM, Ho PP, Han MH, Lanz TV i wsp. Blocking angiotensin-converting enzyme induces potent regulatory T cells and modulates TH1- and TH17-mediated autoimmunity. Proc Natl Acad Sci U S A. 2009; 106:14948-14953.
  • Benkhoucha M, Santiago-Raber ML, Schneiter G, Chofflon M, Funakoshi H, Nakamura T i wsp. Hepatocyte growth factor inhibits CNS autoimmunity by inducing tolerogenic dendritic cells and CD25+Foxp3+ regulatory T cells. Proc Natl Acad Sci U S A. 2010; 107:6424-6429.
  • Hong J, Li N, Zhang X, Zheng B, Zhang JZ. Induction of CD4+CD25+ regulatory T cells by copolymer-I through activation of transcription factor Foxp3. Proc Natl Acad Sci U S A. 2005; 102:6449-6454.
  • Venken K, Hellings N, Thewissen M, Somers V, Hensen K, Rummens JL i wsp. Compromised CD4+ CD25(high) regulatory T-cell function in patients with relapsing-remitting multiple sclerosis is correlated with a reduced frequency of FOXP3-positive cells and reduced FOXP3 expression at the single-cell level. Immunology. 2008; 123:79-89.
  • Frisullo G, Nociti V, Iorio R, Patanella AK, Caggiula M, Marti A i wsp. Regulatory T cells fail to suppress CD4T+-bet+ T cells in relapsing multiple sclerosis patients. Immunology. 2009; 127:418-428.
  • Venken K, Hellings N, Hensen K, Rummens JL, Medaer R, D'hooghe MB i wsp. Secondary progressive in contrast to relapsing-remitting multiple sclerosis patients show a normal CD4+CD25+ regulatory T-cell function and FOXP3 expression. J Neurosci Res. 2006; 83:1432-1446.
  • Haas J, Hug A, Viehöver A, Fritzsching B, Falk CS, Filser A i wsp. Reduced suppressive effect of CD4+CD25high regulatory T cells on the T cell immune response against myelin oligodendrocyte glycoprotein in patients with multiple sclerosis. Eur J Immunol. 2005; 35:3343-3352.
  • Fransson ME, Liljenfeldt LS, Fagius J, Tötterman TH, Loskog AS. The T-cell pool is anergized in patients with multiple sclerosis in remission. Immunology. 2009; 126:92-101.
  • Fletcher JM, Lonergan R, Costelloe L, Kinsella K, Moran B, O'Farrelly C i wsp. CD39+Foxp3+ regulatory T Cells suppress pathogenic Th17 cells and are impaired in multiple sclerosis. J Immunol. 2009; 183:7602-7610.
  • Viglietta V, Baecher-Allan C, Weiner HL, Hafler DA. Loss of functional suppression by CD4+CD25+ regulatory T cells in patients with multiple sclerosis. J Exp Med. 2004; 199:971-979.
  • Kumar M, Putzki N, Limmroth V, Remus R, Lindemann M, Knop D i wsp. CD4+CD25+FoxP3+ T lymphocytes fail to suppress myelin basic protein-induced proliferation in patients with multiple sclerosis. J Neuroimmunol. 2006; 180:178-184.
  • Venken K, Hellings N, Broekmans T, Hensen K, Rummens JL, Stinissen P. Natural naive CD4+CD25+CD127low regulatory T cell (Treg) development and function are disturbed in multiple sclerosis patients: recovery of memory Treg homeostasis during disease progression. J Immunol. 2008; 180:6411-6420.
  • Korporal M, Haas J, Balint B, Fritzsching B, Schwarz A, Moeller S i wsp. Interferon beta-induced restoration of regulatory T-cell function in multiple sclerosis is prompted by an increase in newly generated naive regulatory T cells. Arch Neurol. 2008; 65:1434-1439.
  • Howell OW, Rundle JL, Garg A, Komada M, Brophy PJ, Reynolds R. Activated microglia mediate axoglial disruption that contributes to axonal injury in multiple sclerosis. J Neuropathol Exp Neurol. 2010; 69:1017-1033.
  • Trebst C, König F, Ransohoff R, Brück W, Stangel M. CCR5 expression on macrophages/microglia is associated with early remyelination in multiple sclerosis lesions. Mult Scler. 2008; 14:728-733.
  • Kim S, Steelman AJ, Koito H, Li J. Astrocytes promote TNF-mediated toxicity to oligodendrocyte precursors. J Neurochem. 2011; 116:53-66.
  • Ransohoff RM, Estes ML. Astrocyte expression of major histocompatibility complex gene products in multiple sclerosis brain tissue obtained by stereotactic biopsy. Arch Neurol. 1991; 48:1244-1246.
  • Tzartos JS, Craner MJ, Friese MA, Jakobsen KB, Newcombe J, Esiri MM i wsp. IL-21 and IL-21 Receptor Expression in Lymphocytes and Neurons in Multiple Sclerosis Brain. Am J Pathol. 2011; 178:794-802.
  • Aharoni R. Immunomodulatory drug treatment in multiple sclerosis. Expert Rev Neurother. 2010; 10:1423-1436.
  • Gold R. Oral therapies for multiple sclerosis: a review of agents in phase III development or recently approved. CNS Drugs. 2011; 25:37-52.
  • Tumani H. Corticosteroids and plasma exchange in multiple sclerosis. J Neurol. 2008; 255:36-42.
  • Torkildsen O, Vedeler CA, Ulvestad E, Aarseth JH, Nyland HI, Myhr KM. High dose methylprednisolone induces FcgammaRI on granulocytes in MS-patients. J Neuroimmunol. 2005; 167:138-142.
  • Jalosinski M, Karolczak K, Mazurek A, Glabinski A. The effects of methylprednisolone and mitoxantrone on CCL5-induced migration of lymphocytes in multiple sclerosis. Acta Neurol Scand. 2008; 118:120-125.
  • Blecharz KG, Haghikia A, Stasiolek M, Kruse N, Drenckhahn D, Gold R i wsp. Glucocorticoid effects on endothelial barrier function in the murine brain endothelial cell line cEND incubated with sera from patients with multiple sclerosis. Mult Scler. 2010; 16:293-302.
  • Gelati M, Corsini E, De Rossi M, Masini L, Bernardi G, Massa G i wsp. Methylprednisolone acts on peripheral blood mononuclear cells and endothelium in inhibiting migration phenomena in patients with multiple sclerosis. Arch Neurol. 2002; 59:774-780.
  • Sun YY, Wang CY, Hsu MF, Juan SH, Chang CY, Chou CM i wsp. Glucocorticoid protection of oligodendrocytes against excitotoxin involving hypoxia-inducible factor-1alpha in a cell-type-specific manner. J Neurosci. 2010; 30:9621-9630.
  • Chesik D, De Keyser J. Progesterone and dexamethasone differentially regulate the IGF-system in glial cells. Neurosci Lett. 2010; 468:178-182.
  • Orchinik M, Murray TF, Moore FL. A corticosteroid receptor in neuronal membranes. Science. 1991; 252:1848-1851.
  • Gold R, Buttgereit F, Toyka KV. Mechanism of action of glucocorticosteroid hormones: possible implications for therapy of neuroimmunological disorders. J Neuroimmunol. 2001; 117:1-8.
  • Stahn C, Buttgereit F. Genomic and nongenomic effects of glucocorticoids. Nat Clin Pract Rheumatol. 2008; 4:525-533.
  • Lewis-Tuffin LJ, Cidlowski JA. The physiology of human glucocorticoid receptor beta (hGRbeta) and glucocorticoid resistance. Ann N Y Acad Sci. 2006; 1069:1-9.
  • Barnes PJ. Mechanisms and resistance in glucocorticoid control of inflammation. J Steroid Biochem Mol Biol. 2010; 120:76-85.
  • Tephly LA, Carter AB. Differential expression and oxidation of MKP-1 modulates TNF-alpha gene expression. Am J Respir Cell Mol Biol. 2007; 37:366-374.
  • Quante T, Ng YC, Ramsay EE, Henness S, Allen JC, Parmentier J i wsp. Corticosteroids reduce IL-6 in ASM cells via up-regulation of MKP-1. Am J Respir Cell Mol Biol. 2008; 39:208-217.
  • Turpeinen T, Nieminen R, Moilanen E, Korhonen R. Mitogen-activated protein kinase phosphatase-1 negatively regulates the expression of interleukin-6, interleukin-8, and cyclooxygenase-2 in A549 human lung epithelial cells. J Pharmacol Exp Ther. 2010; 333:310-318.
  • Shepherd EG, Zhao Q, Welty SE, Hansen TN, Smith CV, Liu Y. The function of mitogen-activated protein kinase phosphatase-1 in peptidoglycan-stimulated macrophages. J Biol Chem. 2004; 279:54023-54031.
  • Ito K, Yamamura S, Essilfie-Quaye S, Cosio B, Ito M, Barnes PJ i wsp. Histone deacetylase 2-mediated deacetylation of the glucocorticoid receptor enables NF-kappaB suppression. J Exp Med. 2006; 203:7-13.
  • Gougat C, Jaffuel D, Gagliardo R, Henriquet C, Bousquet J, Demoly P i wsp. Overexpression of the human glucocorticoid receptor alpha and beta isoforms inhibits AP-1 and NF-kappaB activities hormone independently. J Mol Med. 2002; 80:309-318.
  • Ito K, Barnes PJ, Adcock IM. Glucocorticoid receptor recruitment of histone deacetylase 2 inhibits interleukin-1beta-induced histone H4 acetylation on lysines 8 and 12. Mol Cell Biol. 2000; 20:6891-6903.
  • Maneechotesuwan K, Yao X, Ito K, Jazrawi E, Usmani OS, Adcock IM i wsp. Suppression of GATA-3 nuclear import and phosphorylation: a novel mechanism of corticosteroid action in allergic disease. PLoS Med. 2009; 6:e1000076.
  • Schmidt J, Gold R, Schönrock L, Zettl UK, Hartung HP, Toyka KV. T-cell apoptosis in situ in experimental autoimmune encephalomyelitis following methylprednisolone pulse therapy. Brain. 2000; 123:1431-1441.
  • Nguyen KB, McCombe PA, Pender MP. Increased apoptosis of T lymphocytes and macrophages in the central and peripheral nervous systems of Lewis rats with experimental autoimmune encephalomyelitis treated with dexamethasone. J Neuropathol Exp Neurol. 1997; 56:58-69.
  • Barnes PJ, Adcock IM. Glucocorticoid resistance in inflammatory diseases. Lancet. 2009; 373:1905-1917.
  • 218.Lamberts SW. Hereditary glucocorticoid resistance. Ann Endocrinol (Paris). 2001; 62:164-167.
  • 219.Carmichael J, Paterson IC, Diaz P, Crompton GK, Kay AB, Grant IW. Corticosteroid resistance in chronic asthma. Br Med J (Clin Res Ed). 1981; 282:1419-1422.
  • Chikanza IC. Mechanisms of corticosteroid resistance in rheumatoid arthritis: a putative role for the corticosteroid receptor beta isoform. Ann N Y Acad Sci. 2002; 966:39-48.
  • Munkholm P, Langholz E, Davidsen M, Binder V. Frequency of glucocorticoid resistance and dependency in Crohn's disease. Gut. 1994; 35:360-362.
  • Hakonarson H, Bjornsdottir US, Halapi E, Bradfield J, Zink F, Mouy M i wsp. Profiling of genes expressed in peripheral blood mononuclear cells predicts glucocorticoid sensitivity in asthma patients. Proc Natl Acad Sci U S A. 2005; 102:14789-14794.
  • Oakley RH, Jewell CM, Yudt MR, Bofetiado DM, Cidlowski JA. The dominant negative activity of the human glucocorticoid receptor beta isoform. Specificity and mechanisms of action. J Biol Chem. 1999; 274:27857-27866.
  • Rivers C, Levy A, Hancock J, Lightman S, Norman M. Insertion of an amino acid in the DNA-binding domain of the glucocorticoid receptor as a result of alternative splicing. J Clin Endocrinol Metab. 1999; 84:4283-4286.
  • Goleva E, Li LB, Eves PT, Strand MJ, Martin RJ, Leung DY. Increased glucocorticoid receptor beta alters steroid response in glucocorticoid-insensitive asthma. Am J Respir Crit Care Med. 2006; 173:607-616.
  • Kozaci DL, Chernajovsky Y, Chikanza IC. The differential expression of corticosteroid receptor isoforms in corticosteroid-resistant and -sensitive patients with rheumatoid arthritis. Rheumatology (Oxford). 2007; 46:579-585.
  • Orii F, Ashida T, Nomura M, Maemoto A, Fujiki T, Ayabe T i wsp. Quantitative analysis for human glucocorticoid receptor alpha/beta mRNA in IBD. Biochem Biophys Res Commun. 2002; 296:1286-1294.
  • Beger C, Gerdes K, Lauten M, Tissing WJ, Fernandez-Munoz I, Schrappe M i wsp. Expression and structural analysis of glucocorticoid receptor isoform gamma in human leukaemia cells using an isoform-specific real-time polymerase chain reaction approach. Br J Haematol. 2003; 122:245-252.
  • Irusen E, Matthews JG, Takahashi A, Barnes PJ, Chung KF, Adcock IM. p38 Mitogen-activated protein kinase-induced glucocorticoid receptor phosphorylation reduces its activity: role in steroid-insensitive asthma. J Allergy Clin Immunol. 2002; 109:649-657.
  • Ismaili N, Garabedian MJ. Modulation of glucocorticoid receptor function via phosphorylation. Ann N Y Acad Sci. 2004; 1024:86-101.
  • Weigel NL, Moore NL. Steroid receptor phosphorylation: a key modulator of multiple receptor functions. Mol Endocrinol. 2007; 21:2311-2319.
  • Li LB, Goleva E, Hall CF, Ou LS, Leung DY. Superantigen-induced corticosteroid resistance of human T cells occurs through activation of the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK-ERK) pathway. J Allergy Clin Immunol. 2004; 114:1059-1069.
  • Adcock IM, Lane SJ, Brown CR, Lee TH, Barnes PJ. Abnormal glucocorticoid receptor-activator protein 1 interaction in steroid-resistant asthma. J Exp Med. 1995; 182:1951-1958.
  • Matthews JG, Ito K, Barnes PJ, Adcock IM. Defective glucocorticoid receptor nuclear translocation and altered histone acetylation patterns in glucocorticoid-resistant patients. J Allergy Clin Immunol. 2004; 113:1100-1108.
  • Farrell RJ, Murphy A, Long A, Donnelly S, Cherikuri A, O'Toole D i wsp. High multidrug resistance (P-glycoprotein 170] expression in inflammatory bowel disease patients who fail medical therapy. Gastroenterology. 2000; 118:279-288.
  • Hawrylowicz C, Richards D, Loke TK, Corrigan C, Lee T. A defect in corticosteroid-induced IL-10 production in T lymphocytes from corticosteroid-resistant asthmatic patients. J Allergy Clin Immunol. 2002; 109:369-370.
  • Xystrakis E, Kusumakar S, Boswell S, Peek E, Urry Z, Richards DF i wsp. Reversing the defective induction of IL-10-secreting regulatory T cells in glucocorticoid-resistant asthma patients. J Clin Invest. 2006; 116:146-155.
  • Then Bergh F, Kümpfel T, Trenkwalder C, Rupprecht R, Holsboer F. Dysregulation of the hypothalamo-pituitary-adrenal axis is related to the clinical course of MS. Neurology. 1999; 53:772-777.
  • Michelson D, Stone L, Galliven E, Magiakou MA, Chrousos GP, Sternberg EM i wsp. Multiple sclerosis is associated with alterations in hypothalamic-pituitary-adrenal axis function. J Clin Endocrinol Metab. 1994; 79:848-853.
  • van Winsen LM, Polman CH, Dijkstra CD, Tilders FJ, Uitdehaag BM. Suppressive effect of glucocorticoids on TNF-alpha production is associated with their clinical effect in multiple sclerosis. Mult Scler. 2010; 16:500-502.
  • Matysiak M, Makosa B, Walczak A, Selmaj K. Patients with multiple sclerosis resisted to glucocorticoid therapy: abnormal expression of heat-shock protein 90 in glucocorticoid receptor complex. Mult Scler. 2008; 14:919-926.
  • Lehmann HC, Hartung HP, Hetzel GR, Stüve O, Kieseier BC. Plasma exchange in neuroimmunological disorders: Part 1: Rationale and treatment of inflammatory central nervous system disorders. Arch Neurol. 2006; 63:930-935.
  • Sugai S. IgA pyroglobulin, hyperviscosity syndrome and coagulation abnormality in a patient with multiple myeloma. Blood. 1972; 39:224-237.
  • Accorsi P, Passeri C, Onofrillo D, Iacone A. Hyperviscosity syndrome in hematological diseases and therapeutic apheresis. Int J Artif Organs. 2005; 28:1032-1038.
  • Schröder A, Linker RA, Gold R. Plasmapheresis for neurological disorders. Expert Rev Neurother. 2009; 9:1331-1339.
  • Rund D, Schaap T, Gillis S. Intensive plasmapheresis for severe thrombotic thrombocytopenic purpura: long-term clinical outcome. J Clin Apher. 1997; 12:194-195.
  • Frascà G, Vangelista A, DiFelice A, D'Arcangelo GL, Sermasi G, Zucchelli P i wsp. The rationale for plasmapheresis in renal graft rejection. Life Support Syst. 1984; 2:131-136.
  • Yu X, Ma J, Tian J, Jiang S, Xu P, Han H i wsp. A controlled study of double filtration plasmapheresis in the treatment of active rheumatoid arthritis. J Clin Rheumatol. 2007; 13:193-198.
  • Gesinde MO, Tan LB, Gooi HC. Plasma exchange treatment to reduce anti-beta1-adrenergic receptor antibody in a patient with dilated cardiomyopathy. J Clin Apher. 2007; 22:241-242.
  • Mao WL, Chen Y, Chen YM, Li LJ. Changes of Serum Cytokine Levels in Patients With Acute on Chronic Liver Failure Treated by Plasma Exchange. J Clin Gastroenterol. 2010; doi: 10.1097/MCG.0b013e3181faefa3
  • Selset Aandahl G, Jacobsen CD, Rode L, Rathe Oedegaard E. Preliminary experience with plasma exchange in patients with ulcerative colitis. Transfus Sci. 2000; 22:155-160.
  • Gerlag PG, van Rooy MJ, Booij A, van Dam FE, op de Coul AA. Successful treatment by plasmapheresis of respiratory insufficiency in myasthenia gravis. Clin Neurol Neurosurg. 1980; 82:237-243.
  • Valbonesi M, Mosconi L, Garelli S, Zerbi D, Celano I. Successful treatment by plasma exchange in Guillain-Barré syndrome with immune complexes. Vox Sang. 1980; 38:181-184.
  • Färkkilä M, Kinnunen E, Haapanen E, Iivanainen M. Guillain-Barré syndrome: quantitative measurement of plasma exchange therapy. Neurology. 1987; 37:837-840.
  • Höcker P, Stellamor V, Summer K, Mann M. Plasma exchange (PE) and lymphocytapheresis (LCA) in multiple sclerosis (MS). Int J Artif Organs. 1984; 7:39-42.
  • Hauser SL, Dawson DM, Lehrich JR, Beal MF, Kevy SV, Propper RD i wsp. Intensive immunosuppression in progressive multiple sclerosis. A randomized, three-arm study of high-dose intravenous cyclophosphamide, plasma exchange, and ACTH. N Engl J Med. 1983; 308:173-180.
  • Khatri BO, McQuillen MP, Harrington GJ, Schmoll D, Hoffmann RG. Chronic progressive multiple sclerosis: double-blind controlled study of plasmapheresis in patients taking immunosuppressive drugs. Neurology. 1985; 35:312-319.
  • Gordon PA, Carroll DJ, Etches WS, Jeffrey V, Marsh L, Morrice BL i wsp. A double-blind controlled pilot study of plasma exchange versus sham apheresis in chronic progressive multiple sclerosis. Can J Neurol Sci. 1985; 12:39-44.
  • Sørensen PS, Wanscher B, Szpirt W, Jensen CV, Ravnborg M, Christiansen P i wsp. Plasma exchange combined with azathioprine in multiple sclerosis using serial gadolinium-enhanced MRI to monitor disease activity: a randomized single-masked cross-over pilot study. Neurology. 1996; 46:1620-1625.
  • Weiner HL, Dau PC, Khatri BO, Petajan JH, Birnbaum G, McQuillen MP i wsp. Double-blind study of true vs. sham plasma exchange in patients treated with immunosuppression for acute attacks of multiple sclerosis. Neurology. 1989; 39:1143-1149.
  • Weinshenker BG, O'Brien PC, Petterson TM, Noseworthy JH, Lucchinetti CF, Dodick DW i wsp. A randomized trial of plasma exchange in acute central nervous system inflammatory demyelinating disease. Ann Neurol. 1999; 46:878-886.
  • Ruprecht K, Klinker E, Dintelmann T, Rieckmann P, Gold R. Plasma exchange for severe optic neuritis: treatment of 10 patients. Neurology. 2004; 63:1081-1083.
  • Schilling S, Linker RA, König FB, Koziolek M, Bähr M, Müller GA i wsp. Plasma exchange therapy for steroid-unresponsive multiple sclerosis relapses: clinical experience with 16 patients. Nervenarzt. 2006; 77:430-438.
  • Trebst C, Reising A, Kielstein JT, Hafer C, Stangel M. Plasma exchange therapy in steroid-unresponsive relapses in patients with multiple sclerosis. Blood Purif. 2009; 28:108-115.
  • Linker RA, Chan A, Sommer M, Koziolek M, Müller GA, Paulus W i wsp. Plasma exchange therapy for steroid-refractory superimposed relapses in secondary progressive multiple sclerosis. J Neurol. 2007; 254:1288-1289.
  • Cortese I, Chaudhry V, So YT, Cantor F, Cornblath DR, Rae-Grant A. Evidence-based guideline update: Plasmapheresis in neurologic disorders: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2011; 76:294-300.
  • Klingel R, Heibges A, Fassbender C. Plasma exchange and immunoadsorption for autoimmune neurologic diseases - current guidelines and future perspectives. Atheroscler Suppl. 2009;10:129-132.
  • Charlton B, Schindhelm K, Smeby LC, Farrell PC. Analysis of immunoglobulin G kinetics in the non-steady state. J Lab Clin Med. 1985; 105:312-320.
  • Goldammer A, Derfler K, Herkner K, Bradwell AR, Hörl WH, Haas M. Influence of plasma immunoglobulin level on antibody synthesis. Blood. 2002; 100:353-355.
  • Keegan M, König F, McClelland R, Brück W, Morales Y, Bitsch A i wsp. Relation between humoral pathological changes in multiple sclerosis and response to therapeutic plasma exchange. Lancet. 2005; 366:579-582.
  • Wang KC, Wang SJ, Lee CL, Chen SY, Tsai CP. The rescue effect of plasma exchange for neuromyelitis optica. J Clin Neurosci. 2011; 18:43-46.
  • Yoshida H, Ando A, Sho K, Akioka M, Kawai E, Arai E i wsp. Anti-aquaporin-4 antibody-positive optic neuritis treated with double-filtration plasmapheresis. J Ocul Pharmacol Ther. 2010; 26:381-385.
  • Lennon VA, Kryzer TJ, Pittock SJ, Verkman AS, Hinson SR. IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel. J Exp Med. 2005; 202:473-477.
  • Misu T, Fujihara K, Kakita A, Konno H, Nakamura M, Watanabe S i wsp. Loss of aquaporin 4 in lesions of neuromyelitis optica: distinction from multiple sclerosis. Brain. 2007; 130:1224-1234.
  • Khatri BO, Koethe SM, McQuillen MP. Plasmapheresis with immunosuppressive drug therapy in progressive multiple sclerosis. A pilot study. Arch Neurol. 1984; 41:734-738.
  • Dau PC. Increased proliferation of blood mononuclear cells after plasmapheresis treatment of patients with demyelinating disease. J Neuroimmunol. 1990; 30:15-21.
  • Dau PC. Increased antibody production in peripheral blood mononuclear cells after plasma exchange therapy in multiple sclerosis. J Neuroimmunol. 1995; 62:197-200.
  • Medenica RD, Mukerjee S, Alonso K, Lazovic G, Huschart T. Plasmapheresis combined with interferon: an effective therapy for multiple sclerosis. J Clin Apher. 1994; 9:222-227.
  • Yoshii F, Shinohara Y. Natural killer cells in patients with Guillain-Barré syndrome. J Neurol Sci. 1998; 157:175-178.
  • Yoshii F, Shinohara Y. Lymphocyte subset proportions in Guillain-Barré syndrome patients treated with plasmapheresis. Eur Neurol. 2000; 44:162-167.
  • Dau PC. Immunomodulation during treatment of polymyositis with plasmapheresis and immunosuppressive drugs. J Clin Apher. 1994; 9:21-25.
  • Dau PC, Callahan J, Parker R, Golbus J. Immunologic effects of plasmapheresis synchronized with pulse cyclophosphamide in systemic lupus erythematosus. J Rheumatol. 1991; 18:270-276.
  • Dau PC, Callahan JP. Immune modulation during treatment of systemic sclerosis with plasmapheresis and immunosuppressive drugs. Clin Immunol Immunopathol. 1994; 70:159-165.
  • Hanly JG, Hong C, Zayed E, Jones JV, Jones E. Immunomodulating effects of synchronised plasmapheresis and intravenous bolus cyclophosphamide in systemic lupus erythematosus. Lupus. 1995; 4:457-463.
  • Soltész P, Aleksza M, Antal-Szalmás P, Lakos G, Szegedi G, Kiss E. Plasmapheresis modulates Th1/Th2 imbalance in patients with systemic lupus erythematosus according to measurement of intracytoplasmic cytokines. Autoimmunity. 2002; 35:51-56.
  • Baráth S, Soltész P, Kiss E, Aleksza M, Zeher M, Szegedi G i wsp. The severity of systemic lupus erythematosus negatively correlates with the increasing number of CD4+CD25(high)FoxP3+ regulatory T cells during repeated plasmapheresis treatments of patients. Autoimmunity. 2007; 40:521-528.
  • Usnarska-Zubkiewicz L. CD3+ T lymphocytes and interleukin 2 in myelomatous blood hyperviscosity syndrome treated with plasmapheresis. Arch Immunol Ther Exp (Warsz). 1998; 46:317-322.
  • Paglieroni T, Caggiano V, MacKenzie MR. Effects of plasmapheresis on peripheral blood mononuclear cell populations from patients with macroglobulinemia. J Clin Apher. 1987; 3:202-208.
  • Shariatmadar S, Nassiri M, Vincek V. Effect of plasma exchange on cytokines measured by multianalyte bead array in thrombotic thrombocytopenic purpura. Am J Hematol. 2005; 79:83-88.
  • Goto H, Matsuo H, Nakane S, Izumoto H, Fukudome T, Kambara C i wsp. Plasmapheresis affects T helper type-1/T helper type-2 balance of circulating peripheral lymphocytes. Ther Apher. 2001; 5:494-496.
  • Yeh JH, Chien PJ, Hsueh YM, Shih CM, Chiu HC. Changes in the lymphocyte subset after double-filtration plasmapheresis. Am J Clin Pathol. 2007; 128:940-944.
  • Kurtzke JF. Rating neurologic impairment in multiple sclerosis: an expanded disability status scale (EDSS). Neurology. 1983; 33:1444-1452.
  • Nockher WA, Wiemer J, Scherberich JE. Haemodialysis monocytopenia: differential sequestration kinetics of CD14+CD16+ and CD14++ blood monocyte subsets. Clin Exp Immunol. 2001; 123:49-55.
  • Sester U, Sester M, Heine G, Kaul H, Girndt M, Köhler H. Strong depletion of CD14(+)CD16(+) monocytes during haemodialysis treatment. Nephrol Dial Transplant. 2001; 16:1402-1408.
  • Fingerle-Rowson G, Angstwurm M, Andreesen R, Ziegler-Heitbrock HW. Selective depletion of CD14+ CD16+ monocytes by glucocorticoid therapy. Clin Exp Immunol. 1998; 112:501-506.
  • Rzazewska-Makosa B. The mechanism of glucocorticoid resistance in multiple sclerosis. Postepy Hig Med Dosw (Online). 2005; 59:457-463.
  • Linker RA, Gold R. Use of intravenous immunoglobulin and plasma exchange in neurological disease. Curr Opin Neurol. 2008; 21:358-365.
  • Belge KU, Dayyani F, Horelt A, Siedlar M, Frankenberger M, Frankenberger B i wsp. The proinflammatory CD14+CD16+DR++ monocytes are a major source of TNF. J Immunol. 2002; 168:3536-3542.
  • Szaflarska A, Baj-Krzyworzeka M, Siedlar M, Weglarczyk K, Ruggiero I, Hajto B i wsp. Antitumor response of CD14+/CD16+ monocyte subpopulation. Exp Hematol. 2004; 32:748-755.
  • Grage-Griebenow E, Zawatzky R, Kahlert H, Brade L, Flad H, Ernst M. Identification of a novel dendritic cell-like subset of CD64(+) / CD16(+) blood monocytes. Eur J Immunol. 2001; 31:48-56.
  • Rothe G, Gabriel H, Kovacs E, Klucken J, Stöhr J, Kindermann W i wsp. Peripheral blood mononuclear phagocyte subpopulations as cellular markers in hypercholesterolemia. Arterioscler Thromb Vasc Biol. 1996; 16:1437-1447.
  • Weber C, Belge KU, von Hundelshausen P, Draude G, Steppich B, Mack M i wsp. Differential chemokine receptor expression and function in human monocyte subpopulations. J Leukoc Biol. 2000; 67:699-704.
  • Ancuta P, Rao R, Moses A, Mehle A, Shaw SK, Luscinskas FW i wsp. Fractalkine preferentially mediates arrest and migration of CD16+ monocytes. J Exp Med. 2003; 197:1701-1707.
  • Ancuta P, Moses A, Gabuzda D. Transendothelial migration of CD16+ monocytes in response to fractalkine under constitutive and inflammatory conditions. Immunobiology. 2004; 209:11-20.
  • Randolph GJ, Sanchez-Schmitz G, Liebman RM, Schäkel K. The CD16(+) (FcgammaRIII(+)) subset of human monocytes preferentially becomes migratory dendritic cells in a model tissue setting. J Exp Med. 2002; 196:517-527.
  • Fingerle G, Pforte A, Passlick B, Blumenstein M, Ströbel M, Ziegler-Heitbrock HW. The novel subset of CD14+/CD16+ blood monocytes is expanded in sepsis patients. Blood. 1993; 82:3170-3176.
  • Baeten D, Boots AM, Steenbakkers PG, Elewaut D, Bos E, Verheijden GF i wsp. Human cartilage gp-39+,CD16+ monocytes in peripheral blood and synovium: correlation with joint destruction in rheumatoid arthritis. Arthritis Rheum. 2000; 43:1233-1243.
  • Koch S, Kucharzik T, Heidemann J, Nusrat A, Luegering A. Investigating the role of proinflammatory CD16+ monocytes in the pathogenesis of inflammatory bowel disease. Clin Exp Immunol. 2010; 161:332-341.
  • González A, Calleja A, Santiago E, De Miguel C, López-Zabalza MJ, López-Moratalla N. Correlation of activated monocytes or B cells with T lymphocyte subsets in patients with Graves' disease. Int J Mol Med. 1998; 1:95-103.
  • Hanai H, Iida T, Takeuchi K, Watanabe F, Yamada M, Kikuyama M i wsp. Adsorptive depletion of elevated proinflammatory CD14+CD16+DR++ monocytes in patients with inflammatory bowel disease. Am J Gastroenterol. 2008; 103:1210-1216.
  • Zimmermann HW, Seidler S, Nattermann J, Gassler N, Hellerbrand C, Zernecke A i wsp. Functional contribution of elevated circulating and hepatic non-classical CD14CD16 monocytes to inflammation and human liver fibrosis. PLoS One. 2010; 5:e11049.
  • Kanai T, Makita S, Kawamura T, Nemoto Y, Kubota D, Nagayama K i wsp. Extracorporeal elimination of TNF-alpha-producing CD14(dull)CD16(+) monocytes in leukocytapheresis therapy for ulcerative colitis. Inflamm Bowel Dis. 2007; 13:284-290.
  • Subimerb C, Pinlaor S, Lulitanond V, Khuntikeo N, Okada S, McGrath MS i wsp. Circulating CD14(+) CD16(+) monocyte levels predict tissue invasive character of cholangiocarcinoma. Clin Exp Immunol. 2010; 161:471-479.
  • Han J, Wang B, Han N, Zhao Y, Song C, Feng X i wsp. CD14(high)CD16(+) rather than CD14(low)CD16(+) monocytes correlate with disease progression in chronic HIV-infected patients. J Acquir Immune Defic Syndr. 2009; 52:553-559.
  • Azeredo EL, Neves-Souza PC, Alvarenga AR, Reis SR, Torrentes-Carvalho A, Zagne SM i wsp. Differential regulation of toll-like receptor-2, toll-like receptor-4, CD16 and human leucocyte antigen-DR on peripheral blood monocytes during mild and severe dengue fever. Immunology. 2010; 130:202-216.
  • Barisione C, Garibaldi S, Ghigliotti G, Fabbi P, Altieri P, Casale MC i wsp. CD14CD16 monocyte subset levels in heart failure patients. Dis Markers. 2010; 28:115-124.
  • Heine GH, Ulrich C, Seibert E, Seiler S, Marell J, Reichart B i wsp. CD14(++)CD16+ monocytes but not total monocyte numbers predict cardiovascular events in dialysis patients. Kidney Int. 2008; 73:622-629.
  • Urra X, Villamor N, Amaro S, Gómez-Choco M, Obach V, Oleaga L i wsp. Monocyte subtypes predict clinical course and prognosis in human stroke. J Cereb Blood Flow Metab. 2009; 29:994-1002.
  • Moniuszko M, Bodzenta-Lukaszyk A, Kowal K, Lenczewska D, Dabrowska M. Enhanced frequencies of CD14++CD16+, but not CD14+CD16+, peripheral blood monocytes in severe asthmatic patients. Clin Immunol. 2009; 130:338-346.
  • Ulrich C, Heine GH, Garcia P, Reichart B, Georg T, Krause M i wsp. Increased expression of monocytic angiotensin-converting enzyme in dialysis patients with cardiovascular disease. Nephrol Dial Transplant. 2006; 21:1596-1602.
  • Ulrich C, Heine GH, Seibert E, Fliser D, Girndt M. Circulating monocyte subpopulations with high expression of angiotensin-converting enzyme predict mortality in patients with end-stage renal disease. Nephrol Dial Transplant. 2010; 25:2265-2272.
  • Lapteva N, Ide K, Nieda M, Ando Y, Hatta-Ohashi Y, Minami M i wsp. Activation and suppression of renin-angiotensin system in human dendritic cells. Biochem Biophys Res Commun. 2002; 296:194-200.
  • Nahmod K, Gentilini C, Vermeulen M, Uharek L, Wang Y, Zhang J i wsp. Impaired function of dendritic cells deficient in angiotensin II type 1 receptors. J Pharmacol Exp Ther. 2010; 334:854-862.
  • Fertl A, Menzel M, Hofer TP, Morresi-Hauf A, Ziegler-Heitbrock L, Frankenberger M. Monitoring of glucocorticoid therapy by assessment of CD14(+)CD16(+) monocytes: a case report. Immunobiology. 2008; 213:909-916.
  • Dayyani F, Belge KU, Frankenberger M, Mack M, Berki T, Ziegler-Heitbrock L. Mechanism of glucocorticoid-induced depletion of human CD14+CD16+ monocytes. J Leukoc Biol. 2003; 74:33-39.
  • Reder AT, Lowy MT, Meltzer HY, Antel JP. Dexamethasone suppression test abnormalities in multiple sclerosis: relation to ACTH therapy. Neurology. 1987; 37:849-853.
  • Reder AT, Makowiec RL, Lowy MT. Adrenal size is increased in multiple sclerosis. Arch Neurol. 1994; 51:151-154.
  • Erkut ZA, Hofman MA, Ravid R, Swaab DF. Increased activity of hypothalamic corticotropin-releasing hormone neurons in multiple sclerosis. J Neuroimmunol. 1995; 62:27-33.
  • Correale J, Gilmore W, Li S, Walsh J, Bassani MM, Lund B i wsp. Resistance to glucocorticoid-induced apoptosis in PLP peptide-specific T cell clones from patients with progressive MS. J Neuroimmunol. 2000; 109:197-210.
  • DeRijk RH, Eskandari F, Sternberg EM. Corticosteroid resistance in a subpopulation of multiple sclerosis patients as measured by ex vivo dexamethasone inhibition of LPS induced IL-6 production. J Neuroimmunol. 2004; 151:180-188.
  • van Winsen LM, Muris DF, Polman CH, Dijkstra CD, van den Berg TK, Uitdehaag BM. Sensitivity to glucocorticoids is decreased in relapsing remitting multiple sclerosis. J Clin Endocrinol Metab. 2005; 90:734-740.
  • Ysrraelit MC, Gaitán MI, Lopez AS, Correale J. Impaired hypothalamic-pituitary-adrenal axis activity in patients with multiple sclerosis. Neurology. 2008; 71:1948-1954.
  • van Winsen LM, Hooper-van Veen T, van Rossum EF, Koper JW, Barkhof F, Polman CH i wsp. Glucocorticoid receptor gene polymorphisms associated with more aggressive disease phenotype in MS. J Neuroimmunol. 2007; 186:150-155.
  • van Winsen LM, Manenschijn L, van Rossum EF, Crusius JB, Koper JW, Polman CH i wsp. A glucocorticoid receptor gene haplotype (TthIII1/ER22/23EK/9beta) is associated with a more aggressive disease course in multiple sclerosis. J Clin Endocrinol Metab. 2009; 94:2110-2114.
  • van Winsen LL, Hooper-van Veen T, van Rossum EF, Polman CH, van den Berg TK, Koper JW i wsp. The impact of glucocorticoid receptor gene polymorphisms on glucocorticoid sensitivity is outweighted in patients with multiple sclerosis. J Neuroimmunol. 2005; 167:150-156.
  • Zettl UK, Hartung HP, Pahnke A, Brueck W, Benecke R, Pahnke J. Lesion pathology predicts response to plasma exchange in secondary progressive MS. Neurology. 2006; 67:1515-1516.
  • a
Document Type
paper
Publication order reference
Identifiers
YADDA identifier
bwmeta1.element.psjd-2ffc3a48-a218-47bf-b852-f90845380c4c
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.