T cell receptor usage in rheumatoid arthritis.
The structure of alpha beta T cell receptors (TCR) is restricted in a number of rodent and human antigen responses. In several rodent EAE models of multiple sclerosis a limited range of T cell receptors are expressed by T cells which respond to the inciting antigen and are capable of transferring the disease to naive animals. These observations have raised the question of whether in rheumatoid arthritis (RA), a particular T cell receptor structural signature can be identified among T cells derived from the synovium compared to autologous peripheral blood. The parameters which are usually measured are TCR variable region usage, oligoclonality and/or limited junctional region usage. A large number of studies have been carried out and results are variable with some authors claiming evidence for the effect of uncharacterised superantigens expanding or deleting T cells with particular V beta regions while others have suggested that observations of restricted V region usage and limited junctional regions imply that clones of cells have been expanded by antigen. So far none of these studies have led to the identification of an antigen or superantigen which plays a role in RA pathogenesis.
Lanchbury
J S
JS
Molecular Immunogenetics Unit, Division of Medicine, United Medical and Dental Schools, Guy's Hospital, London, UK.
Hall
M A
MA
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D015329:Gene Rearrangement, T-Lymphocyte; D006801:Humans; D008285:Major Histocompatibility Complex / Q000276:immunology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology*
D016693:Receptors, Antigen, T-Cell, alpha-beta