Rheumatology Advance Access published online on February 28, 2003
Rheumatology, doi:10.1093/rheumatology/keg097
Rheumatology © British Society for Rheumatology 2003; all rights reserved
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Review
1 University of Cambridge School of Clinical Medicine, Department of Medicine, Cambridge, UK
* Corresponding author. E-mail: lhb22{at}cam.ac.uk.
Received 8 May 2002
; accepted 8 August 2002
Despite extensive research, it remains unclear why a small proportion of HLA- B27+ individuals develop spondyloarthropathies (SpA). Because the function of HLA-B27, as a major histocompatibility complex (MHC) class I molecule, is peptide presentation to CD8+ T cells, research has concentrated on the role of HLA-B27 as a restriction element for CD8+ cytotoxic T lymphocytes in pathogenesis. However, findings in the B27-transgenic animal models, together with the identification of unusual processing and presentation features of HLA-B27, have raised alternative hypotheses for the pathogenic role of HLA-B27. One such hypothesis is that HLA-B27 can be recognized by CD4+ T lymphocytes. Here we report the identification of such unusual cells, which break the conventional rules of MHC restriction, and propose a model for the role of such CD4+ T cells in SpA.
Key words: Major histocompatibility complex, Spondyloarthropathy, HLA-B27, T lymphocytes.
Breaking the rules: the unconventional recognition of HLA-B27 by CD4+ T lymphocytes as an insight into the pathogenesis of the spondyloarthropathies
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