The structure of alpha beta T cell receptors (TCR) is restricted in a
number of rodent and human antigen responses. In several rodent EAE mo
dels of multiple sclerosis a limited range of T cell receptors are exp
ressed by T cells which respond to the inciting antigen and are capabl
e of transferring the disease to naive animals. These observations hav
e raised the question of whether in rheumatoid arthritis (RA), a parti
cular T cell receptor structural signature can be identified among T c
ells derived from the synovium compared to autologous peripheral blood
. The parameters which are usually measured are TCR variable region us
age, oligoclonality and/or limited junctional region usage. A large nu
mber of studies have been carried out and results are variable with so
me authors claiming evidence for the effect of uncharacterised superan
tigens expanding or deleting T cells with particular V beta regions wh
ile others have suggested that observations of restricted V region usa
ge and limited junctional regions imply that clones of cells have been
expanded by antigen. So far none of these studies have led to the ide
ntification of an antigen or superantigen which plays a role in RA pat
hogenesis.