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HLA Class II Molecules (hla + class_ii_molecule)

Distribution by Scientific Domains

Medical Sciences	100%

Distribution within Medical Sciences

Neurology	50%
Immunology	25%

Selected Abstracts

Immunoglobulin IgG Fc-receptor polymorphisms and HLA class II molecules in Guillain,Barré syndrome

ACTA NEUROLOGICA SCANDINAVICA, Issue 1 2010
S. Sinha
Sinha S, Prasad KN, Jain D, Nyati KK, Pradhan S, Agrawal S. Immunoglobulin IgG Fc-receptor polymorphisms and HLA class II molecules in Guillain,Barré syndrome. Acta Neurol Scand: 2010: 122: 21,26. © 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Objective,,, To analyze host genetic factors immunoglobulin G Fc receptors (Fc,Rs) and human leukocyte antigen (HLA) class II in GBS patients. Methods,,, Fc,RIIA, IIIA and IIIB polymorphisms were studied in 80 each GBS patients and healthy controls by allele specific PCR. HLA class II DR,1 and DQ,1 typing was performed at the two-digit level by PCR in randomly selected 54 GBS patients and 202 controls. Results,,, Fc,RIIA-H/H (56% vs 9%; P < 0.0001) and Fc,RIIIA-V/V (40% vs 13%; P < 0.0001) genotypes, H131 allele frequencies (0.73 vs 0.26, P < 0.0001) and HLA DQ,1*060x (OR, 1.96; 95% CI, 1.26,3.04; P < 0.01) were significantly increased in GBS than controls. DR,1*0701 alone (OR, 10; 95% CI, 45.90,2.25; P < 0.001) and together with Fc,RIIA-H/H (OR, 11.03; 95% CI, 2.63,46.20; P < 0.001) was significantly associated with GBS patients having microbiological evidence of recent infection. Conclusions,,, The study indicates that homozygous Fc,RIIA and Fc,RIIIA genotypes and Fc,RIIA H131 allele are associated with GBS. HLA class II molecule DR,1*0701 is identified as novel genetic risk factor for development of GBS in patients with preceding infection. [source]

Disease-related epitope spread in a humanized T cell receptor transgenic model of multiple sclerosis

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 7 2004
Stephan Ellmerich
Abstract While EAE has been an invaluable model for the immunopathogenesis of multiple sclerosis, it has sometimes been difficult to bridge the gap between findings and therapies in the rodent models and the cellular and molecular interactions that can be studied in the human disease. Humanized transgenic models offer a means of achieving this, through the expression of disease-implicated HLA class II molecules, co-expressed with a cognate HLA-class II-restricted, myelin-specific TCR derived from a human T cell clone implicated in disease. We have generated such a transgenic line, called line 8, that co-expresses a high level of HLA-DR15 and a human TCR specific for HLA-DR15/MBP 85,99. T cells from the transgenic line are skewed to the CD4 single-positive compartment and produce IFN-, in response to peptide from mylein basic protein. Mice develop a spontaneous disease phenotype, showing poverty of movement, although this rarely develops into paralysis except following immunization with peptide. On induction of paralysis by immunization with peptide, disease correlates with epitope spread to a number of additional, HLA-DR15-restricted myelin epitopes. This model should be valuable for analyzing epitope spread in a humanized immunogenetic environment and for the testing of specific immunotherapies. [source]

Evidence for Humoral Rejection of a Pancreatic Islet Graft and Rescue with Rituximab and IV Immunoglobulin Therapy

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2009
L. Kessler
We describe the decline in islet function, in relation to HLA sensitization, in an islet transplant recipient and the recovery of this function after treatment with anti-CD20 monoclonal antibody and IV immunoglobulins. A 51-year-old woman with type 1 diabetes received one intraportal islet infusion. Following this transplantation, she became insulin independent. A search for HLA antibodies by using an ELISA technique remained consistently negative for HLA class I and II. It was only 2 years after the islet transplantation that this search became positive against class II antigens, reaching a peak of reactivity concomitantly with the appearance of a deterioration of glucose control requiring low-dose insulin therapy. Luminex® screening and single-antigen assays then revealed the presence of both nondonor-specific and donor-specific antibodies against HLA class II molecules. This immunization, already present in the pretransplant serum, had increased during the 6 months preceding the clinical deterioration. Since these data nevertheless pointed to antibody-mediated rejection of the islet allograft, treatment with anti-CD20 monoclonal antibody and IV immunoglobulins was initiated. One month later, the search by ELISA for antibodies against HLA class II antigens became negative, the Luminex® tests normalizing more gradually. As the result of an improvement in glucose control, the patient was again insulin-free. [source]

Human leukocyte antigen-DR15, low infant sibling exposure and multiple sclerosis: Gene,environment interaction

ANNALS OF NEUROLOGY, Issue 2 2010
Ingrid A. F. van der Mei
The risk for development of multiple sclerosis has been associated with human leukocyte antigen-DRB1*1501-DQB1*0602 (HLA-DR15) genotype, low infant sibling exposure, and high Epstein,Barr nuclear antigen IgG levels. In a population-based case,control study (Tasmania, Australia), we found that the combined effect of HLA-DR15 positivity and low infant sibling exposure on multiple sclerosis (odds ratio, 7.88; 95% confidence interval, 3.43,18.11) was 3.9-fold greater than expected (test for interaction, p = 0.019) This interaction was observed irrespective of Epstein,Barr nuclear antigen IgG levels. This suggests that immune mechanisms involving HLA class II molecules are susceptible to modulation in early life. Ann Neurol 2009;66:261,265 ANN NEUROL 2010;67:259,263 [source]

Proinflammatory mediator,induced reversal of CD4+,CD25+ regulatory T cell,mediated suppression in rheumatoid arthritis

ARTHRITIS & RHEUMATISM, Issue 3 2007
Jocea M. R. van Amelsfort
Objective We previously demonstrated that CD4+,CD25+ regulatory T (Treg) cells are present in increased numbers in the synovial fluid (SF) of rheumatoid arthritis (RA) patients and display enhanced suppressive activity as compared with their peripheral blood (PB) counterparts. Despite the presence of these immunoregulatory cells in RA, chronic inflammation persists. The purpose of the present study was to investigate whether particular proinflammatory mediators that are associated with RA could abrogate CD4+,CD25+ Treg,mediated suppression. Methods Monocyte phenotype was determined by flow cytometry and cytokine levels by enzyme-linked immunosorbent assay. Magnetically sorted CD4+,CD25, and CD4+,CD25+ T cells derived from the PB and SF obtained from RA patients were stimulated alone or in coculture with anti-CD3 monoclonal antibody (mAb) and autologous antigen-presenting cells, in the absence or presence of anti-CD28 mAb or the proinflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor , (TNF,), or IL-7. Results Monocytes from the SF of RA patients displayed increased expression of HLA class II molecules, CD80, CD86, and CD40 as compared with PB-derived monocytes, indicating their activated status. Mimicking this increased costimulatory potential, addition of anti-CD28 mAb to cocultures of CD4+,CD25, and CD4+,CD25+ T cells resulted in reduced CD4+,CD25+ Treg,mediated suppression in both PB and SF. Furthermore, IL-7 and, to a limited extent, TNF,, both of which are produced by activated monocytes and were detected in SF, abrogated the CD4+,CD25+ Treg,mediated suppression. In contrast, IL-6 did not influence Treg-mediated suppression. Conclusion Our findings suggest that the interaction of CD4+,CD25+ Treg cells with activated monocytes in the joint might lead to diminished suppressive activity of CD4+,CD25+ Treg cells in vivo, thus contributing to the chronic inflammation in RA. [source]

Immunoglobulin IgG Fc-receptor polymorphisms and HLA class II molecules in Guillain,Barré syndrome

High-affinity human leucocyte antigen class I binding variola-derived peptides induce CD4+ T cell responses more than 30 years post-vaccinia virus vaccination

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2009
M. Wang
Summary Interferon-, secreting T lymphocytes against pox virus-derived synthetic 9-mer peptides were tested by enzyme-linked immunospot in peripheral blood of individuals vaccinated with vaccinia virus more than 30 years ago. The peptides were characterized biochemically as high-affinity human leucocyte antigen (HLA) class I binders (KD , 5 nM). However, five of the individuals tested did not show typical CD8+ T cell-mediated HLA class I-restricted responses. Instead, these donors showed CD4+ T cell-dependent responses against four of a total of eight antigenic 9-mer peptides discovered recently by our group. These latter responses were blocked specifically in the presence of anti-HLA class II antibody. We conclude that long-lived memory responses against pox virus-derived 9-mer peptides, with high binding affinity for HLA class I molecules, are mediated in some cases by CD4+ T cells and apparently restricted by HLA class II molecules. [source]