Learn about the flu shot, COVID-19 vaccine, and our masking policy »
New to MyHealth?
Manage Your Care From Anywhere.
Access your health information from any device with MyHealth. You can message your clinic, view lab results, schedule an appointment, and pay your bill.
ALREADY HAVE AN ACCESS CODE?
DON'T HAVE AN ACCESS CODE?
NEED MORE DETAILS?
MyHealth for Mobile
Get the iPhone MyHealth app »
Get the Android MyHealth app »
Abstract
Rheumatoid arthritis is characterized by a strong HLA-DRB1 association and a histologic picture consistent with an antigen recognition event by tissue-infiltrating T cells. Basic immunology has seen major progress in the understanding of the T-cell receptor-MHC-antigen interaction; however, the role of T cells and disease-associated HLA-DRB1 alleles in rheumatoid arthritis remains elusive. Recent studies on the genetics of the HLA-DRB1 association and the diversity of the repertoire of synovial T cells, and treatment studies with T-cell depleting antibodies, have suggested that the model of T cells recognizing an arthritogenic antigen in association with a HLA-DR molecule is too simplistic. The findings are more consistent with a regulatory role of T cells. Patients with rheumatoid arthritis have a unique T-cell repertoire that not only reflects the influence of disease-associated HLA-DRB1 alleles but also is greatly skewed by the clonal expansion of few CD4+ and CD8+ T-cell specificities. Understanding these repertoire changes appears to be promising not only in permitting understanding of the pathogenesis of this disease but also in designing T-cell-targeted treatment strategies.
View details for Web of Science ID A1995RQ40500005
View details for PubMedID 8619093