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1

Immunotherapy of rheumatoid arthritis targeting inflammatory cytokines and autoreactive T cells

100%
Chen G.
Archivum Immunologiae et Therapiae Experimentalis
|
2010
|
vol. 58
|
issue 1
27-36
EN
Rheumatoid arthritis is a chronic disorder for which there is no known cure. Concentrating on specific elements of the abnormal immune response that characterizes the disease, scientists are reaching into biotechnology's bag of tricks to develop immunotherapeutic techniques. This paper will present some advances in the immunotherapy of rheumatoid arthritis targeting inflammatory cytokines and autoreactive T cells.
2

Quantification of the CD8+ T cell response against a mucin epitope in patients with breast cancer

100%
Kokowski K., Harnack U., Dorn D. C., Pecher G.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 2
141-145
EN
Mucin 1, encoded by the MUC1 gene, is a tumor-associated antigen expressed on the surface of breast cancer cells. It would be of interest to see whether there is a naturally existing T cell immune response against mucin epitopes in cancer patients. Materials and Methods: Using tetramer and interferon gamma assays, the immune response to one MUC1 peptide epitope in the peripheral blood of breast cancer patients was quantified. The data were compared with the clinical course of the patients. Results: CD8+ T cells capable of recognizing the HLA-A*0201-restricted STAPPVHNV epitope were detected in 9 of 19 patients with a frequency ranging 0.01?0.082%. No significant difference was found between the occurrence of epitope-specific CD8+ T cells of patients with progressive disease and disease-free patients. However, all patients with stable disease showed a specific immune response, including both patients with the highest frequency. Conclusions: The results of this study provide further evidence that a natural specific cellular immune response against this mucin epitope exists in breast cancer patients.
3

Cytokine-producing T cell subsets in human leishmaniasis

100%
Kemp K.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
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vol. 48
|
issue 3
173-176
EN
Leishmania specific Th1/Th2 cells have been identified in humans as well as in mice. There is a correlation between the clinical outcome of the infection and the cytokine response profile. Generally, the production of Th2 cytokines leads to severe infection, whereas the production of Th1 cytokines leads to subclinical or mild infections. In mice, an infection leads to a polarisation of either Th1 or Th2 Leishmania antigen specific cells. In contrast, both Th1 and Th2 Leishmania antigen specific cells can be identified in humans cured from L. donovani infections. Theoretically, Th1 cells and Th2 cells mutually down-regulate each other. However, the presence of antigen specific regulatory T cell subsets may provide an environment that allows the presence of both Th1 and Th2 cells.
4

Treatment of autoimmune disease: time for a paradigm shift?

100%
Mor F.
Archivum Immunologiae et Therapiae Experimentalis
|
2007
|
vol. 55
|
issue 1
13-18
EN
Current treatment of human autoimmune diseases (AIDs) was developed empirically and relies mostly on non-selective suppression of the immune system. Traditional non-selective immunosuppressants such as corticosteroids, cyclophosphamide, and methotrexate and more novel means such as monoclonal antibodies to CD3, CD4, or CD25 do not discriminate between pathogenic and beneficial T cells. Importantly, the severe side effects seen with current therapies are related to the fact that these treatments not only suppress the pathogenic disease-inducing cells, but also cells influential in combating infections and killing malignant cells. Severe infections and malignancies are the inevitable result of non-selective immune suppression. Many of the novel forms of therapy of AID were developed in experimental animals, and their translation to the human disease was associated with the revelation of unexpected and sometimes catastrophic side effects. These surprises underscore the major differences between the relative simplicity of the experimental model and the complexity of the human disease. How can this current state of treatment of AID be improved? Which principles should guide us in the design of new treatments? This review attempts to offer a new look at these questions.
5

The physiological role of regulatory T cells in the prevention of autoimmunity: generation, specificity and mode of action

100%
Seddon B.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 5
339-346
EN
Until recently, the traditional view was that tolerance to self antigens was maintained by a combination of physical deletion intrathymically and functional deletion in the periphery of autoreactive T cells. There is now, however, abundant evidence that the normal T cell repertoire contains overtly autoreactive T cells whose pathogenic potential is held in check by the activity of a distinct subset of peripheral T cells, so called regulatory or suppressor T cells. This article examines data from one model of rodent autoimmunity, where autoimmune pathology develops following thymectomy and irradiation of normal laboratory rats, which characterise the development and function of these so called regulatory T cells.
6

Role of lipid rafts in T cells

100%
Thomas S., Kumar R., D_ B. T.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
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vol. 52
|
issue 4
215-224
EN
The plasma membrane of T cells is made up of a combination of phospholipids and proteins organized as glycolipoprotein microdomains termed lipid rafts. The structural assembly of lipid rafts was investigated by various physical and biochemical assays. Depending on the differentiation status of T cells, the lipid rafts seclude various protein receptors instrumental for the early T cell signaling, cytoskeleton reorganization, protein and membrane trafficking, and the entry of infectious organisms into the cells. This review article summarizes recent information on the assembly of lipid rafts in plasma membrane of T cells and their signaling output in mature and thymic precursors towards cell growth and differentiation, and possible modalities by which the function of lipid rafts can be altered by drugs and T cell ligands. The concept of using lipid rafts as a target for pharmaceutical compounds and biological T cell ligands to ultimately alter the T cell function is discussed.
7

Cytokine signaling/transcription factor cross-talk in T Cell activation and Th1-Th2 differentiation

100%
Liberman A. C., Refojo D., Arzt E.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
|
issue 6
351-366
EN
The secretion of interleukin (IL)-2 is a key event in T cell activation. IL-2 allows T cells to enter into the S phase of the cell cycle and divide. After the activation phase takes place, T lymphocytes proliferate and differentiate to generate effector T cells. Thereby, T helper (Th) precursor cells, which are functionally immature, may become Th1 or Th2 effector cells. These subsets are responsible for cell-mediated immunity and humoral responses, respectively. Both, T cell activation and Th differentiation are processes that depend on changes in the pattern of gene expression. The expression and changes in the genes responsible for these events are regulated by transcription factors. This review will focus on both transcription factors involved in the control of IL-2, as well as those that are key in T helper differentiation.
8

Staphylococcal superantigens: do they play a role in sepsis?

100%
Holtfreter S., Broker B. M.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 1
13-27
EN
In Staphylococcus aureus, 19 different superantigens (SAgs) have been described. Their genes are all located on mobile genetic elements, such as pathogenicity islands, plasmids, and phages. SAgs bypass conventional antigen recognition by directly cross-linking major histocompatibility complex class II (MHCII) molecules on antigen-presenting cells with T cell receptors. This leads to massive T cell proliferation and cytokine release, which may end in toxic shock syndrome. The role of SAgs in other forms of sepsis is less well defined. In animal models, SAgs and lipopolysaccharide (LPS) very efficiently synergize in the induction of lethal shock, and on the basis of these observations a two-hit model of sepsis has been proposed: LPS or another monocyte stimulus hits first, then SAg or another T cell stimulus hits. In clinical studies, however, evidence for an involvement of SAgs in sepsis has been difficult to obtain. This may have a number of reasons: differences between humans and rodents in their response to LPS and SAg, heterogeneity of SAg combinations in S. aureus clinical isolates, lack of tools to analyze SAg effects in patients, blocking anti-SAg serum antibodies, and MHCII polymorphisms.
9

Induction and maintenance of self tolerance: the role of CD4+CD25+ regulatory T cells

100%
Bala K. K., Moudgil K. D.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 5
307-321
EN
The immune system responds vigorously to invading pathogens (non-self, foreign), while remaining unresponsive (tolerant) to the body's own components and circulating constituents (self). This indifference to self components is a result of finely orchestrated events of thymic negative selection (central tolerance) of developing T cells that are autoaggressive combined with those operative in the periphery (peripheral tolerance) to control the activity of potentially autoreactive T cells that escaped thymic tolerance. Recently, autoimmune regulator expressed in the thymus has been identified as a critical mediator of central tolerance towards tissue-specific antigens. In the periphery, a variety of regulatory T cells are involved in effecting tolerance. There is immense interest and excitement about the newly identified subset of CD4+CD25+ T cells. This is a unique subset of CD4+ T cells that bear CD25 (IL-2Ra chain) on the cell surface in the na?ve state and express FoxP3 as a unique marker. These cells suppress the activity of autoreactive effector T cells primarily via cell-cell contact. The deficiency and/or altered function of CD4+CD25+ T cells is associated with autoimmunity. Mice deficient in FoxP3 (scurfy mice) bear an autoimmune phenotype, and human males with mutations in the corresponding gene express the phenotype of widespread autoimmunity, the immune dysregulation, polyendocrinopathy and enteropathy, and X-linked syndrome. In vitro expansion of antigen-specific CD4+CD25+ T cells and their adoptive transfer into patients suffering from autoimmunity is emerging as a promising new therapeutic approach for these debilitating disorders. Development of tolerance to self antigens involves processes occurring within the thymus (central tolerance) and at extra-thymic sites (peripheral tolerance).
10

Anti-GBM glomerulonephritis: a T cell-mediated autoimmune disease?

100%
Lou Y.-H.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 2
96-103
EN
Anti-glomerular basement membrane (GBM) glomerulonephritis, which was among the earliest recognized human autoimmune diseases, is characterized by the presence of anti- -GBM antibody. It has been a prototypical example of autoantibody-mediated autoimmune disease. However, decades of research on this disease, based either on clinical observations or experimental models, have revealed that T cell-mediated cellular immunity may potentially be a more important mediator of glomerulonephritis. We have made several breakthroughs in understanding the T cell-mediated mechanism causing this disease in a rat model based on Goodpasture's antigen, non-collagen domain 1 of ?3 chain of type IV collagen (Col4alpha3NC1). We demonstrated that anti-GBM glomerulonephritis was induced by either passive transfer of Col4alpah3NC1-specific T cells or active immunization with the nephritogenic T cell epitope of Col4alpha3NC1. Immunization with the T cell epitope also triggered production of anti-GBM antibodies to diversified GBM antigens. Thus, a single nephritogenic T cell epitope alone is sufficient to induce the clinical spectrum of anti-GBM glomerulonephritis, including proteinuria, glomerular injury, and anti-GBM antibody. A possible T cell-mediated mechanism for causing human anti-GBM disease is proposed.
11

Lymphocytes distribution and intrahepatic compartmentalization during HCV infection: a main role of MHC-unrestricted T cells

100%
Agrati C., Nisii C., Oliva A., D?Offizi G., Montesano C., Pucillo L. P., Poccia F.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 5
307-316
EN
Hepatitis-C virus (HCV) infection induces an acute and chronic liver inflammation through an immune mediated pathway that may lead to cirrhosis and liver failure. Indeed, HCV-related hepatitis is characterized by a dramatic lymphocyte infiltrate in the liver which is mainly composed by HCV non-specific cells. Several data indicated that IFN-gamma secretion by intrahepatic lymphocytes (IHL) may drive non specific cell homing to the liver inducing IP-10 production. An interesting hallmark of these IHL is the recruitment of lymphocytes associated with mechanism of innate immunity such as NK, NKT and gamma delta T lymphocytes. CD81 triggering on NK cell surface by the HCV envelope glycoprotein E2 was recently shown to inhibit NK cell function in the liver of HCV-infected persons resulting in a possible mechanism contributing to the lack of virus clearance and to the establishment of chronic infection. In contrast, intrahepatic NKT cells restricted to Cd1d molecules expressed on the hepatocyte surface may contribute to a large extent to the liver damage. Finally, an increased frequency of T cell expressing the gamma delta TCR was observed in HCV-infected liver and recent observations indicate that intrahepatic gamma delta T cell activation could be directly induced by the HCV/E2 particle through CD81 triggering. These cells are not HCV specific, are able to kill target cells including primary hepatocytes and their ability to produce Th1 cytokines is associated with an higher degree of liver disease. Altogether, CD1d/NKT and/or E2/CD81 interactions may play a major role in the establishment of HCV immunopathogenesis. In absence of virus clearance, the chemokine-driven recruitment of lymphocytes with an innate cytotoxic behavior in the liver of HCV infected patients may boost itself leading to the necroinflammatory and fibrotic liver disease.
12

T cell depleted haploidentical bone marrow transplantation for the treatment of children with severe combined immunodeficiency

100%
Smogorzewska E. M., Brooks J., Annett G., Kapoor N., Crooks G. M., Kohn D. B., Parkman R., Weinberg K. I., D. B. K.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 2
111-118
EN
Severe combined immunodeficiency (SCID) is fatal in early childhood if unrecognized and if not treated. The aim was to determine the efficacy of T cell depleted bone marrow transplantation (TCD BMT) in the treatment of children with SCID. Eleven children diagnosed with SCID received histocompatible related donor bone marrow transplantation ? HRD BMT (group I). Thirty seven children diagnosed with SCID who did not have histocompatible donors were treated with TCD haploidentical parental bone marrow transplantation (BMT) (group II). TCD was performed by in vitro soybean lectin agglutination followed by E-rosette depletion. Patients were longitudinally assessed for the presence and function of T and B lymphocytes. In group I all children survived. The mean age of children in this group at the time of HRD BMT was 15. 4 months. All surviving patients normalized their specific T cell function. Two out of 11 require treatment with intravenous immunoglobulin i. v. Ig. In group II 17 out of 37 (46%) children survived. At the time of TCD BMT the mean age of survivors was 7. 5 months, vs. 11. 4 months in patients who died. Death was caused most commonly by opportunistic infections, Epstein-Barr virus induced lymphoproliferative disease (EBV-LPD), and graft versus host disease (GvHD). Seventeen out of 17 surviving patients recovered normal numbers of CD3+ cells and antigen specific T cell function. Five out of 17 never recovered their B cell function and require i. v. Ig injections. Early diagnosis, prevention or treatment of opportunistic infections, and enhancement of immune recovery will be necessary to improve survival in patients with SCID treated with TCD BMT.
13

Development and selection of T Cells: how many subsets? how many rules?

100%
Kisielow P.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 6
407-414
EN
Since the discovery indicating that thymus derived lymphocytes (T cells) can be divided into two subpopulations: CD8+ (killer) and CD4+ (helper) cells, subsequent studies revealed bewildering heterogeneity of T cells. In the present review an attempt is made to present the actual picture of T cell heterogeneity, introduce some order into nomenclature and summarize the rules behind the development and selection of different, currently recognized T cell subsets.
14

CD30 expression on allergen- and non-allergen-specific T cell lines and its role in cytokine production

100%
M. T.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 5
335-343
EN
The main interest in CD30 has mainly focused on its ability to discriminate between T helper (Th)2 and Th1 subpopulations. The role of CD30 as the marker for Th2 cells is still controversial, which may be due to the fact that the expression and the role of CD30 is not fully understood. The data presented in this paper provides information on the expression and activity of CD30 in T cell lines specific to allergen or tuberculin-purified protein derivative (PPD) as the model of Th2 or Th1 responses, respectively. The results have shown that CD30 expression was the highest on T cells stimulated with antigen in the presence of interleukin (IL)-12 and it was present on both cell lines, regardless of antigen specificity. Activation of the CD30 receptor on CD4+ T cells, however, showed differences in mRNA expression for IL-4 between these cells. IL-4 mRNA was induced by CD30 costimulation at the same level as was obtained with anti-CD28 agonistic antibodies in allergen-specific T cells. In PPD-specific T cells this effect was not observed. Additionally, there was no effect of anti-CD30 stimulation on IL-6 mRNA expression in any of the cell lines. Comparison of protein cytokine levels for IL-4 and interferon (IFN)-gamma have shown that the highest production of IL-4 was obtained from allergen-specific T cells costimulated with anti-CD28. Although this effect was much lower in the case of CD30 costimulation, it was still above that the anti-CD3 activation alone. No effect of CD30 activation was observed in regard of IFN-gamma mRNA or protein expression in any cell line. The results of the study showed that CD30 receptor is not exclusively present on Th2 cells; however its activity may promote a Th2-dependent reaction by modulating IL-4 production.
15

Uncovering the differences between T cell tolerance and immunity

100%
Vella A. T.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 5
331-338
EN
In the last two decades T cell function has been analyzed in vitro from many different angles with a great deal of attention dedicated to the basic requirements of activation. During this time a compendium of information has been collected and has proven to be invaluable. Paradoxically very little is known about T cell activation and function in vivo. In the last decade a number of models have been developed which allow the tracking of Ag-activated T cells in vivo and these studies have been instrumental in advancing the field of T cell biology. In particular, a new and emerging paradigm of T cell immunity is evolving.
16

Epitope spreading: a mechanism for progression of autoimmune disease

100%
Tuohy V. K., Kinkel P.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 5
347-352
EN
Autoimmune diseases are typically characterized by a persistent inflammatory self-recognition process that ultimately leads to chronic progressive disability. Over the past several years we have addressed the fundamental question of why autoimmune diseases are chronic. Our working hypothesis in these studies has been that autoimmunity involves a continuous acquisition of new self-recognition events, thereby providing an inflammatory steady-state that leads to chronicity. This acquired T cell neoautoreactivity is commonly referred to as epitope spreading. By studying mulitple sclerosis (MS) and its related animal model, experimental autoimmune encephalomyelitis (EAE), we have found that chronic progression of autoimmune disease is invariably linked to the development of any epitope-spreading process that manifests as a cascade of inflammatory T cell neoautoreactivities to a sequential series of predictable new target self-antigens. However, our most recent observations indicated that the emergence of epitope spreading is accompanied by a concurrent regression of the established primary autoreactivity associated with disease onset. Thus, our studies indicate that progression of autoimmune disease involves a shifting of T cell autoreactivity from primary initiating self-determinants to defined cascades of secondary determinants that sustain the inflammatory self-recognition process during progression to chronicity. Our data support the view that the natural development of self-recognition during autoimmune disease may best be understood when considered in the temporal context of an ?epitope du jour? and ?moving target? perspective.
17

The molecular mechanisms of post-adhesive transmigration of T cells

100%
Masuyama J.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 2
121-128
EN
Leukocyte extravasation is an essential phenomenon in inflammatory responses of the body. However, less is known about the mechanisms of transendothelial migration of leukocytes subsequent to their adhesion to the endothelium. It could be considered that at least three different cellular responses participate in the transmigration of adherent leukocytes: 1) polarization of adherent cells in cell shape, 2) interactions between adherent cells and molecules bound to the endothelial surface to stimulate migration through the junction between adjacent endothelial cells, and 3) co-ordination with endothelial cells to open the junction. Molecules involved in these events are discussed in this review.
18

Human T cell leukemia virus type 1: the role of Tax in leukemogenesis

100%
Pise-Masison C. A., Jeong S.-J., Brady J. N.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 4
283-296
EN
Human T cell leukemia virus type 1 (HTLV-1) is a complex human retrovirus which is the causative agent of adult T cell leukemia (ATL). ATL occurs in about 4% of carriers and develops after a long latent period. Although the precise mechanism of HTLV-1 oncogenesis remains unclear, the pathogenesis has been linked to the pleiotropic activity of the viral transcriptional activator protein Tax. Tax has been shown to regulate viral and cellular gene expression and to functionally interfere with proteins involved in cell-cycle progression and DNA repair. This review will focus on the role of Tax in p53 inhibition.
19

Regulation of innate and adaptive immune responses by the related cytokines IL-12, IL-23, and IL-27

100%
Beadling C., Slifka M. K.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 1
15-24
EN
The functional characterization and subsequent purification of T cell growth factor/interleukin (IL)-2 in the early 1980s established this secreted protein as a key mediator of immune cell activation and provided the prototype that enabled the discovery of numerous cytokines over the ensuing two decades. While soluble immunoregulatory factors were initially identified functionally as biological activities present in the culture supernatants of activated lymphocytes/monocytes, this methodology shifted radically following the completion of the human genome sequence. Computer-generated structural modeling algorithms have replaced functional assays and biochemical purification as the initial means of discovering new cytokines. To date, a total of 31 interleukins, as well as over a dozen other related hematopoietic factors, have been identified. These cytokines and their receptors may be grouped on the basis of structural homologies as well as by shared ligand and receptor subunits. The challenge now at hand is to define the biological functions of the newly identified cytokines and to elucidate the common and divergent roles of related family members. This point is well illustrated by the IL-12/IL-23/IL-27 family, whose members share ligand and receptor subunits and play somewhat overlapping roles in innate and adaptive immune responses. These three cytokines are not entirely redundant, as they may preferentially activate na?ve or memory T cells, induce discrete T cell cytokine profiles, contribute to distinct stages of host immune responses to infectious agents, and differentially promote autoimmunity. Further elucidation of the unique functions of the IL-12 family members may lead to improved immunodiagnostics and therapies.
20

NK T Cell-NK cell cross-talk: reciprocal interaction and activation?

100%
Wesley J., Brossay L.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 2
121-126
EN
Initiation and propagation of the immune response is the result of a series of coordinated cellular and biochemical interactions that lead to the activation of multiple cell types. It is now clear that an optimal immune response requires a precise and rapid communication between different cell subsets. This phenomenon, referred to as cross-talk, is believed to be an essential component of the immune response that provides necessary inflammatory mediators and cytolytic activity for controlling infections and diseases. An example of an effective cooperation between different cell types has been recently illustrated by the finding that specific activation of CD1 restricted natural killer T cells (NK T) can quickly lead to the activation of other subsets of cells such as natural killer (NK) and CD8 T cells.
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