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Rheumatology 2000; 39: 458-462
© 2000 British Society for Rheumatology


Editorials

Tracking T cells in arthritis

L. R. Wedderburn

Departments of Rheumatology and Molecular Pathology, University College London, Windeyer Institute of Medical Sciences, 46 Cleveland Street, London W1P 6DB, UK

The first 150 words of the full text of this article appear below.

In the 25 yr since the demonstration that specific recognition of antigens by T lymphocytes requires interaction with a self major histocompatibility complex (MHC) molecule [1], significant advances have been made in our understanding of this process. Initial observations of MHC associations with autoimmune disease involved the class I allele HLA-B27 with spondyloarthropathies in both adults and children [2, 3]. Subsequently, part of the inherited susceptibility to other arthritides was mapped to the MHC, in particular the association of severe rheumatoid arthritis (RA) with class II genes coding for HLA-DRß molecules [4, 5], which share a common sequence in positions 67–74 [6]. Strong associations with MHC DRB1 alleles have also been recognized in the chronic arthritides of children, now collectively known as juvenile idiopathic arthritis (JIA). These differ from the RA-associated alleles and map to specific subgroups of disease, such . . . [Full Text of this Article]


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