The British Journal of Rheumatology, Vol 36, 622-629, Copyright © 1997 by British Society for Rheumatology
T Sumida, I Matsumoto, T Maeda and K Nishioka
Studies on the TCR repertoire of T cells in several inflamed lesions of SS
patients have shown that there exist no unique TCR V family genes, although
TCR V gene usage is relatively restricted. Analysis of the clonality of
infiltrating T cells shows that some T cells expand clonally in lesions,
suggesting that these cells were induced by antigen-driven rather than
superantigen-driven stimulation. The restricted usage of the TCRJ beta, V
alpha and J alpha genes also supports the notion that all expanded T cells
do not accumulate due to superantigen. Junctional sequence analysis has
revealed some conserved amino acid sequence motifs in the TCR CDR3 region,
which is the antigen- binding site on T cells. These observations strongly
suggest that pathogenic T cells in lesions recognize limited epitopes on
autoantigens in the context of HLA. These findings are similar to TCR on T
cells in rheumatoid synovium, as described elsewhere [51]. Intriguingly, T
cells in lacrimal and labial salivary glands recognize common epitopes, but
T cells in the kidney react with different autoantigens from those in minor
salivary glands. In the future, the peptides recognized by pathogenic
autoreactive T cells should be clarified to elucidate the mechanism for the
progression of SS. Moreover, we predict that a vaccination with analogue
peptides, to induce autoreactive T cells to anergy, might provide a new
strategy for the specific treatment of SS.
REVIEWS
T-cell receptor in Sjogren's syndrome
Division of Rheumatology and Molecular Immunology, St Marianna University School of Medicine, Kawasaki, Japan.
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