Rheumatology 2000; 39: 458-462
© 2000 British Society for Rheumatology
Editorials |
Tracking T cells in arthritis
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 6774 [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