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1

New insights into the pathophysiology and in vivo function of IgG Fc receptors through gene deletion studies

100%
Baumann U., Schmidt R. E., Gessner J. E.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
|
issue 6
399-406
EN
Fc-receptors for IgG (Fc gammaRs) are critically involved at multiple stages of an immune response, ranging from antigen presentation and regulation of antibody production to the end-stage effector mechanisms of inflammation. Immunolglobulin G autoantibodies that are detectable in the majority of autoimmune diseases are ligands for Fc gammaRs. The three classes, Fc gammaRI, Fc gammaRII, and Fc gammaRIII, vary in their antibody affinity, cellular expression and in vivo function. We review the current knowledge on regulation and diverse functions of the distinct Fc gammaRs and describe the evidence of their important immunoregulatory roles in autoimmunity based on recent work in animal models.
2

Interleukin 15: Its role in inflammation and immunity

100%
Perera L. P.
|
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vol. 48
|
issue 5
457-464
EN
Interleukin-15 (IL-15) is a 14-15 kDa polypeptide that belongs to the four alpha-helix bundle family of cytokines and was originally discovered due to its T cell proliferative activity. It utilizes the signal transducing b/g polypeptides of the IL-2 receptor complex thus sharing many biological activities with IL-2, in addition to its high affinity private receptor subunit IL-15Ra. Accumulating evidence indicates that the biological relevance of IL-15 may not solely be confined to T lymphocytes, but to a variety of cell populations within the immune system as well as outside the immune system of the host. The expression of both IL-15 and its high affinity receptor component, IL-15Ra are readily demonstrable in a wide variety of tissues and appear to be augmented in response to environmental/stress stimuli and infectious agents. There is increasing evidence to suggest that IL-15 may play an important role in protective immune responses, allograft rejection and the pathogenesis of autoimmune diseases where mononuclear cell infiltration is a hallmark feature. Herein, the effects of IL-15 on cells associated with host defense, immunity and inflammation are reviewed and support a central role for this cytokine in orchestrating multiple aspects of effector functions in immunity and inflammation.
3

Immunotherapy in the management of sepsis

100%
Sikora J. P.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
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issue 5
317-324
EN
The work presents the role of Gram-negative bacteria endotoxins, pro- and anti-inflammatory cytokines and reactive oxygen species (ROS) in the complex and not fully explained pathogenesis of sepsis. The so called ?respiratory burst? of neutrophils and antioxidant mechanisms of the host are also discussed. The work has focused on possible approaches to the management of sepsis connected with immunotherapy. Neutralisation of endotoxin lypopolysaccharide (LPS), anti-TNF-alpha therapy with monoclonal antibodies or pentoxifylline (PTXF) as well as soluble recombinant cytokine agonists and antagonists used in clinical trials were taken into consideration. Besides, cytokine manipulation therapy, anti-adhesion techniques or glicocorticoides and antioxidant barrier interference were also described. So far there has been no immunotherapy of sepsis in children of proven clinical efficacy, which prompts aggressive examination of the immune system, aimed at affecting its function.
4

The common gamma c-cytokines and transplantation tolerance

100%
Vu M. D., Li X. C.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 4
267-273
EN
Transplant rejection, like tolerance, is a T cell-dependent event. There is compelling evidence to suggest that induction of transplant tolerance is an actively learned process in which T cells need to engage the alloantigens in order to learn to tolerate the allograft. A family of cytokines whose receptors use the same IL-2 receptor gamma chain (also called the common gamma c) plays an important role in regulating multiple aspects of the allograft response (i.e. rejection vs. tolerance). It is undeniable that gamma c-cytokines can drive clonal expansion and effector maturation of alloreactive T cells, and therefore, targeting such cytokines or their receptor components remains an attractive way of blocking transplant rejection. However, we just started to appreciate that gamma c-cytokines also regulate the acquisition of transplant tolerance via programming activated T cells for apoptotic cell death and via guiding the evolution of regulatory T cells. Thus, understanding precisely the role of gamma c-cytokines in regulating T cell homeostasis and T cell regulation is critically important in the induction of transplant tolerance.
5

Regulation of local immunity by airway epithelial cells

100%
Mayer A. K., Dalpke A. H.
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2007
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vol. 55
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issue 6
353-363
EN
Epithelial cells are the first line of defense against invading microbial pathogens. They are important contributors to innate mucosal immunity and generate various and sophisticated anti-microbial defense mechanisms, including the formation of a tight barrier and secretion of anti-microbial substances as well as inflammatory mediators. To provide these active defense mechanisms, epithelial cells functionally express various pattern-recognition receptors. Toll-like receptors have been shown to recognize conserved microbial patterns mediating inducible activation of innate immunity. Mucosal surfaces, however, are prone to contact with pathogenic as well as non-pathogenic microbes and, therefore, immune-recognition principles have to be strictly regulated to avoid uncontrolled permanent activation. This review will focus on mechanisms by which epithelial cells regulate mucosal immune responses, thus creating an organ-specific microenvironment. This includes local adaptations in microbial recognition, regulation of local immune homeostasis, and modulation of antigen-presenting cells and adaptive immune responses. These regulatory mechanisms serve the special needs of controlled microbial recognition in mucosal compartments.
6

iNOS expression and NO production by neutrophils in cancer patients

100%
Jablonska E., Puzewska W., Marcinczyk M., Grabowska Z.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
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issue 2
175-179
EN
The tumor-polymorphonuclear neutrophil (PMN) relationship can be altered by the release of toxic molecules, such as nitric oxide (NO). The aim of the present study was to examine the expression of the inducible synthase of NO (iNOS) and NO production by human neutrophils of patients with oral cavity cancer. For comparison we performed similar examinations in autologous peripheral blood mononuclear cells (PBMCs). PMNs and PBMCs were isolated from the whole blood of 27 patients with squamous cell carcinoma of the oral cavity. iNOS protein expression in these cells was detected by Western blot. Total nitrite as an indicator of NO concentrations in the culture supernatants and the serum of patients was measured using a colorimetric assay. The PMNs of oral cavity cancer patients showed a significantly lower intensity of iNOS expression than those of healthy controls. The PBMCs of patients showed a more intensive expression of iNOS than the PMNs, but a lower intensity than the PBMCs of the controls. The expression of iNOS in rhIL-6 and rhIL-15-stimulated PMNs and PBMCs of patients increased in comparison with unstimulated cells. We observed lower productions of NO by PMNs and PBMCs of patients than those of the control group. The results revealed that altered iNOS expression and NO production are more characteristic of PMNs than of PBMCs of patients with oral cavity cancer. Additionally, this study provided new information about IL-6 and IL-15 activity in a tumor-bearing host.
7

Immunotherapy of inflammatory bowel diseases: current concepts and future perspectives

100%
Neurath M. F.
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|
vol. 48
|
issue 2
81-84
EN
The etiology and the pathogenesis of inflammatory bowel diseases (IBD), e. g. Crohn's disease and ulcerative colitis are still not completely understood. However, there is growing evidence that an alteration of the mucosal immune system towards luminal antigens in a genetically susceptible host plays a key role in the pathogenesis of IBD. In particular, cytokines produced by intestinal epithelial cells, lamina propria macrophages and CD4+ T cells appear to contribute to the initiation and perpetuation of intestinal inflammation in IBD. This review focuses on the role of the mucosal immune system in the pathogenesis of IBD and potential novel immunotherapeutic strategies for chronic intestinal inflammation. Such strategies include recombinant antiinflammatory cytokines, neutralizing antibodies or fusion proteins, antisense oligonucleotides and adenoviral gene transfer.
8

Viruses as hijackers of PML nuclear body

100%
Moller A., Schmitz M. L.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
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issue 5
295-300
EN
Promyelocytic leukemia nuclear bodies (PML-NBs) are discrete interchromosomal macromolecular structures. The integrity of this dynamic nuclear subcompartment critically depends on the presence of the name-giving PML protein. Among the permanent or transient residents of PML-NBs are various regulatory proteins, including Sp100, CBP, pRb, HIPK2, RAD51 and p53. PML-NBs are frequently targeted by viral infections, as a number of different RNA and DNA viruses including herpesviruses, adenoviruses, papovaviruses, papillomaviruses and arenaviruses cause changes in PML-NBs. Viruses interfere with PML-NB in two ways: 1) some viral proteins can associate with PML-NB proteins and/or lead to the destruction and lysis of this subnuclear compartment, thus aiding viral gene expression and disabling the host's innate immunity; 2) the parental genomes of some nuclear-replicating DNA viruses associate preferentially with PML-NBs, which presumably serves to assist in viral gene expression or replication. Here we feature the different viral strategies leading to the hijacking of PML-NBs and discuss the consequences for the immune response.
9

Are NKT cells essential for endotoxic shock?

100%
Emoto M.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
|
issue 4
231-236
EN
Endotoxic shock is a major health threat caused by Gram-negative bacteria and their unique cell wall component, lipopolysaccharide which induces exaggerated production of proinflammatory cytokines. Although macrophages play a central role in the pathogenesis of endotoxic shock, NK1+ cells are also involved in this mechanism. NK1+ cells comprise two major populations, namely NK cells and NKT cells. It remains, however, elusive whether either NK cells, NKT cells or both are involved in induction of endotoxic shock. This review will focus on the relative contribution of these NK1+ cells to the pathogenesis of endotoxic shock.
10

Rho kinase in the regulation of cell death and survival

100%
Shi J., Wei L.
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2007
|
vol. 55
|
issue 2
61-75
EN
Rho kinase (ROCK) belongs to a family of serine/threonine kinases that are activated via interaction with Rho GTPases. ROCK is involved in a wide range of fundamental cellular functions, such as contraction, adhesion, migration, and proliferation. Recent studies have shown that ROCK plays an important role in the regulation of apoptosis in various cell types and animal disease models. Two ROCK isoforms, ROCK1 and ROCK2, are assumed to be function redundant, this based largely on kinase construct overexpression and chemical inhibitors (Y27632 and fasudil) which inhibit both ROCK1 and ROCK2. Gene targeting and RNA interference approaches allow further dissection of distinct cellular, physiological, and patho-physiological functions of the two ROCK isoforms. This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of ROCK signaling in the regulation of apoptosis and highlights new findings from recently generated ROCK-deficient mice.
11

Allergen-specific T lymphocytes as targets for specific immunotherapy: striking at the roots of type I allergy

100%
Bohle B.
|
|
issue 4
233-242
EN
In the past decades allergic diseases have tremendously increased and hypersensitivity reactions now represent a growing health concern in industrialized countries. Despite various effective therapeutic options for the treatment of allergic diseases, only specific immunotherapy (SIT) has been shown to have effects on the underlying immunological mechanisms, namely functional changes at the level of T helper lymphocytes (Th). It was found that allergen-specific CD4+ Th2 lymphocytes play a key role in the pathophysiology of atopic diseases. During successful SIT, the Th2-dominated immune response is modified towards a Th1 response, leading to a decline in allergen-specific IgE levels in the long term. In order to improve the efficacy and safety of SIT, novel approaches were developed targeting allergen-specific Th2 lymphocytes since specific inactivation or modulation towards Th1 cells could interfere with the disease process. In view of this aspect, this review will basically focus on two new promising approaches to improve SIT: 1) the use of hypoallergenic proteins characterized by reduced IgE-binding capacities but retained T lymphocyte-activating properties and 2) oligodeoxynucleotides containing CpG motifs as an example of adjuvants which foster Th1 immune responses. Both approaches promise to be capable of adjusting the pathological Th2 immune response.
12

Concentration of TBA-reactive substances in type II pneumocytes exposed to oxidative stress

100%
Piotrowski W. J., Marczak J., Kurmanowska Z., Gorski P.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 6
435-440
EN
Oxidative lung damage may be associated with the destruction of alveolar cells. Type II alveolar epithelial cells (AECs), as progenitors of type I cells, are indispensable for the renovation of alveolar structure after lung injury. Extensive damage to type II cells could be responsible for unfavorable outcome. However, the susceptibility of type II AECs to oxidative stress is unclear. Materials We investigated the susceptibility of freshly isolated and cultured rat type II AECs to and Methods: oxidative stress (H2O2 and Fe2+). Thiobarbituric acid reactive substances (TBARS) were measured as indices of lipid peroxidation and cytotoxicity was estimated by the MTT test. Aminotriazol (ATZ), an inhibitor of intracellular catalase, was used to estimate the protective role of catalase. Results: TBARS concentration increased significantly in freshly isolated, oxidant-exposed cells (4.0?1.3 vs. 8.3?2.2 nmol/g protein, p=0.0313) and insignificantly in cultured cells (1.7?0.4 vs. 4.4?1.7 nmol/g protein). ATZ was toxic even to cells not exposed to oxidants. Inhibition of catalase in cells exposed to oxidants resulted in an insignificant increase in TBARs: 4.5?1.5 vs. 16.2?3.9 nmol/g protein, p=0.0625, and 4.0?0.8 vs.7.6?4.0 for freshly isolated and cultured cells, respectively. Oxidative stress itself did not increase cytotoxicity. Conclusions: Type II AECs are not resistant to oxidative stress. We cannot, however, explain why cells with evidence of lipid peroxidation do not show increased cytotoxicity. The toxicity of ATZ is not related to oxidative cell damage. In cells exposed to oxidants, TBARS may further increase when catalase is inhibited, which suggests an important protective role for catalase.
13

Prevalence of the intron 22 inversion of the factor VIII gene and inhibitor development in Polish patients with severe hemophilia A

100%
Sawecka J., Skulimowska J., Windyga J., Lopaciuk S., Koscielak J.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 4
352-356
EN
Patients with severe hemophilia A often develop inhibitors (antibodies) against transfused factor VIII. One hundred thirteen Polish patients with severe hemophilia A, who had been treated on demand with cryoprecipitate until 1992 and exclusively with factor VIII concentrates after 1995, were examined for intron 22 inversion by Southern blotting and the presence and magnitude of inhibitor activity in blood as determined by the Bethesda assay. The patients' ages ranged 4?67 years (mean: 33.7?12.4 years, median: 32 years). The number of patients with the inversion amounted to 57, while in 56 patients the mutation types were unknown; 47 patients had a distal and 10 patients a proximal type of inversion. Thirteen patients with inversions (22.8%) were found to have inhibitor in their blood. Most patients (14 out of 15) who developed inhibitors in the course of cryoprecipitate therapy were high responders. Conversely, 4 of 5 patients treated between 1992 and 1995 with both cryoprecipitate and intermediate-purity factor VIII concentrates were low responders. One multitransfused patient who had remained inhibitor-free on cryoprecipitate therapy developed inhibitor after receiving a large dose of factor VIII concentrate during surgery. None of these 5 patients developed inhibitors during their 12?40 years of treatment with cryoprecipitate, suggesting that it was less immunogenic than factor VIII concentrates. The prevalence of the intron 22 inversion mutation of the factor VIII gene in Polish hemophiliacs is similar to that in other European countries. Treatment regimens with either cryoprecipitate or virus-inactivated plasma-derived Factor VIII concentrates may affect inhibitor formation in hemophilia A patients.
14

Human sera with precipitating antibodies to human soluble immune complexes. A brief communication

100%
Milgrom F., Czechowski D.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 3
197-200
EN
Previous numerous papers by the senior author dealt with the human serum factor referred to as anti-antibody which is specifically directed against IgG antibodies that underwent molecular transformation in the course of the reactions with their corresponding antigens. The reactions of this serum factor could be conveniently detected by means of agglutination of Rh-positive erythrocytes sensitized by anti Rh antibodies. No precipitation tests could be developed.Most studies were conducted by means of double diffusion in gel precipitation. Most studies were conducted by means of double diffusion in gel precipitation.Sera with precipitating anti-antibodies may serve as exquisite reagents for detection of soluble immune complexes in human sera.
15

Preventing staphylococcal disease by disarming the immune responses to infection

100%
Tarkowski A.
|
|
vol. 48
|
issue 1
21-26
EN
Use of experimental models of staphylococcal infections clarified several bacterial virulence factors as well as many hematopoetic cell types and their products that are involved in the pathogenesis of infection. For many decades it has been believed that antibody mediated response to staphylococci and their products was the major, if not the only one, hallmark of immune reactivity during infection. Recent studies have documented that T cell mediated responses to superantigens produced by staphylococci are not only prominent but also decisive with respect to sequels. Also the nonantigen specific immune responsiveness to staphylococcal infection is reviewed including roles of neutrophils, complement system and nitric oxide. The knowledge gained regarding staphylococcal virulence factors and the host immune responses has prompted researchers to develop new strategies how to interact in vivo witl the infectious process. Some of these approaches are commented in this review regarding e. g. vaccination procedures in order to prevent severe infections as well as therapeutic procedures to minimize organ damage during an ongoing infectious process.
16

A direct comparison of rejection by CD8 and CD4 T cells in a transgenic model of allotransplantation

100%
Porrett P. M., Lee I. M. K., Lian M. M., Wang J., Caton A. J., Deng S., Markmann J. E., Moore D. J.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 3
192-200
EN
Introduction: The relative contributions of CD4+ and CD8+ T cells to transplant rejection remains unknown. The authors integrated a previous model of CD4-mediated graft rejection with a complementary model of CD8-mediated rejection to directly compare the function of graft-reactive CD4+ and CD8+ lymphocytes in vivo in a model where rejection requires transgenic T cells. These studies allow direct comparison of CD4 and CD8 T cell responses to the same antigen without the confounding effects of T cell depletion or homeostatic proliferation. Materials and Methods: Clone 4 and TS1 mice possess MHC class I- and II-restricted CD8+ and CD4+ T cells, respectively, which express transgenic T cell receptors that recognize the influenza hemagglutinin antigen (HA). We compared the in vivo response of CFSE-labeled, HA-specific transgenic CD8+ and CD4+ T cells after adoptive transfer into syngeneic BALB/c mice grafted with HA-expressing skin. Results: As in the authors' CD4+ model, HA104 skin was consistently rejected by both Clone 4 mice (n=9, MST: 14.2) and by 5x105 Clone 4 lymphocytes transferred to naive BALB/c hosts that do not otherwise reject HA+ grafts. Rejection correlated with extensive proliferation of either graft-reactive T cell subset in the draining lymph nodes, and antigen-specific CD4+ and CD8+ cells acquired effector function and proliferated with similar kinetics.Conclusions: These data extend the authors' unique transgenic transplantation model to the investigation of CD8 T cell function. The initial results confirm fundamental functional similarity between the CD4 and CD8 T cell subsets and provide insight into the considerable redundancy underlying T cell mechanisms mediating allograft rejection.
17

Neuro-endocrine-immune axis in human rheumatoid arthritis

100%
Sakane T., Suzuki N.
|
|
vol. 48
|
issue 5
417-428
EN
We present an overview of the role of neuro-endocrine-immune mechanisms in the pathophysilogical responses of patients with rheumatoid arthritis (RA). In patients with RA proinflammatory cytokines secreted by synovial cells provoke local inflammation in the joints and, simultaneously, initiate a systemic acute phase response. Thus, profund changes of the neuro-endocrine-immune axis could take place in the patients. Defects in the hypothalamus-pituitary-adrenal axis have been observed in patients with RA. Prolactin levels are often elevated and a abnormal sex hormone levels have been described in RA patients. Defective neural regulation of inflammation involving neuropeptides at least partly plays a pathogenic role in RA.We and others have found that participants of the neuro-endocrine-immune interactions, such as hormones, neurotransmitters and neuropeptides, modulate RA synovial cell functions and that they are actually produced by, and their receptors are expressed on, cells within the inflammatory joint compartment. Thus, neuropeptides and hormones not only affect a systemic acute phase response of RA patients, but also modulate local inflammation directly in RA joints. These results suggest that defects in regulatory processes, which are fundamental to RA, may lie in the immune system, the nervous system, the endocrine system or the interactions of these. A better understanding of neuro-endocrine-immune interactions holds the promise of new approaches to the treatment of RA with the use of hormones, neurotransmitters, neuropeptides and/or their antagonists.
18

17beta-estradiol treatment profoundly down regulates gene expression in spinal cord tissue in mice protected from experimental autoimmune encephalomyelitis

100%
Matejuk A., Dwyer J., Hopke C., Vandenbark A. A., Offner H.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 3
185-193
EN
It is now well documented that experimental autoimmune encephalomyeltitis (EAE) can be effectively prevented by estrogen therapy. Previously, we identified a limited set of genes that were altered in spleens of mice protected from EAE by 17-estradiol (E2) treatment. As a continuation of these studies, we here present transcriptional changes in genes expressed in spinal cord tissue. The Affymetrix microarray system was used to screen more than 12,000 genes from E2-treated double Tg (BV8S2 and AV4) female mice protected from EAE vs. control mice with severe EAE. We found that estrogen therapy had a profound inhibitory effect on expression of many immune-related genes in spinal cords. Estrogen significantly affected transcription of 315 genes, 302 that were down-regulated and only 13 that were up-regulated by >2.4 fold. A number of genes encoding the histocompatibility complex, cytokines/receptors, chemokines, adhesion molecules, and signal transduction proteins, were strongly down regulated (>20 fold) in estrogen treated mice to levels similar to spinal cord tissue from unmanipulated mice. The identification of genes with altered expression patterns in spinal cords of estrogen treated mice provides unique insight into the process that ultimately results in protection against EAE.
19

Evasion of host immune surveillance by hepatitis c virus: potential roles in viral persistence

100%
Moorman J. P., Joo M., Hahn J. S.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 3
189-194
EN
Hepatitis C virus (HCV) is a major human pathogen that causes mild to severe liver disease worldwide. This positive strand RNA virus is remarkably efficient at establishing chronic infections. In order for a noncytopathic virus such as HCV to persist, the virus must escape immune recognition or evade host immune surveillance. Immune escape via the hypervariable region of the E2 envelope protein has been postulated as one mechanism for HCV persistent infection. Such hypervariability within the E2 protein may be under selective pressure from protective B cell or T cell responses and be able to escape immune recognition by rapid mutation of antigenic site. In addition to antigenic variation, HCV may also suppress immune response, leading to dampening of cellular immunity. This is supported by recent studies in our laboratory demonstrating that the HCV core protein can suppress host immune responses to vaccinia virus by downregulating viral specific cytotoxic T lymphocyte (CTL) responses and cytokine production. An understanding of the mechanisms behind HCV persistence will provide a basis for the rational design of vaccines and novel therapeutic agents targeting human HCV infection.
20

Epstein-Barr virus association in pediatric abdominal non-Hodgkin-lymphomas from Turkey

100%
Tinguely M., Brundler M.-A., Gogus S., Kerl K., Borisch B.
|
|
vol. 48
|
issue 4
317-322
EN
Recent sudies have shown marked geographic variation associated with Epstein-Barr virus (EBV) in pediatric Burkitt's lymphomas and Hodgkin's disease. In the present study we investigated 30 cases of pediatric extranodal high grade non-Hodgkin's lymphomas (NHL) from Turkey with an abdominal localisation. To classify them histologically and to determine the role of EBV in these lymphomas, immunohistochemistry (IHC), in situ hybridisation (ISH) and polymerase chain reaction (PCR) were used. Our series contained two histologic types: the Burkitt's or Burkitt's-like lymphomas (BL/BLL) and high grade NHL. They all were of the B cell type. The immunoglobulin heavy chain gene rearrangement revealed monoclonality in 87% of the BL/BLL cases, in contrast to the NHL cases, showing monoclonality in only 43% of the cases. EBV was found in tumor cells in a high frequency, independent of the histological subtype. EBV strains A and B were detected in 9 cases, with a preponderance of the B subtype (4/9 BL/BLL; 4/9 NHL). Our data suggest that high grade NHLs with abdominal localisation of Turkish children show the pattern of immunodeficient lymphomas to some extent.
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