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Molecular basis for the association between HLA DR4 and rheumatoid arthritis. From the shared epitope hypothesis to a peptidic model of rheumatoid arthritis

✍ Scribed by Salvatore Albani; Jean Roudier

Publisher: Elsevier Science
Year: 1992
Tongue: English
Weight: 354 KB
Volume: 25
Category: Article
ISSN: 0009-9120
DOI: 10.1016/0009-9120(92)90328-p

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✦ Synopsis

Susceptibility to rheumatoid arthritis (RA) maps to residues QKRAA/QRRAA in the third hypervariable region of the HLA DRI31 chain. Peptides from the same area of MHC class II molecules are able to modulate the T-cell repertoire by deleting self-reactive T-cells. The Epstein Barr virus glycoprotein gp110 and the dna J heat-shock protein from E. coil mimic the third hypervariable region of HLA-Dw4DRI31. Thus, the same area of HLA DR[31 carries susceptibility to RA, modulates the T-cell repertoire and is mimicked by human pathogens. RA may originate from a particular shape imposed on the T-cell repertoire by the QKRAA/QRRAA sequence in the third hypervariable region of HLA DRy1.

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