Association of rheumatoid arthritis with an amino acid allelic variation of the T cell receptor
✍ Scribed by F. Cornélis; L. Hardwick; R. M. Flipo; M. Martinez; S. Lasbleiz; J. F. Prud' Homme; T. H. Tran; S. Walsh; A. Delaye; A. Nicod; M. N. Loste; V. Lepage; K. Gibson; K. Pile; S. Djoulah; P. M. Danzé; F. Lioté; D. Charron; J. Weissenbach; D. Kuntz; T. Bardin; B. P. Wordsworth
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 376 KB
- Volume
- 40
- Category
- Article
- ISSN
- 0004-3591
No coin nor oath required. For personal study only.
✦ Synopsis
To investigate allelic variations of T cell receptor residues for a contribution to rheumatoid arthritis (RA) susceptibility.
Methods.
We conducted an RA case-control study involving 1,579 northwest Europeans: 766 patients with erosive and rheumatoid factor-positive disease and 813 control subjects. Productive changes of segments TCRAV6S1, TCRAV7S1, TCRAVSSl, TCRAVlOS2, and TCRBV6S1, TCRBV6S7 were investigated by singlestrand conformation polymorphisms. The TCRAVSSl association was confirmed by restriction fragment length polymorphism.
Results. In the systematic study (77 patients and 119 controls), an increase in 1 TCRAVSSl genotype was found in the RA patients (P = 0.0004). This finding was replicated in 2 further populations, one from France
📜 SIMILAR VOLUMES
Objective. To analyze the CD4؉ ؉ ؉ T cell responses to the human cartilage antigen glycoprotein-39 (HCgp-39) in the context of rheumatoid arthritis (RA)-associated (DR␣1\*0401) and nonassociated (DR␣1\*0402) HLA class II molecules. Methods. Large numbers of HCgp-39-specific T cell hybridomas were