Open AccessAn abnormal T cell repertoire in hypergammaglobulinaemic primary Sjogren's syndrome
Author(s) -
KAY R. A.,
HAY E. M.,
DYER P. A.,
DENNETT C.,
GREEN L. M.,
BERNSTEIN R. M.,
HOLT P. J. L.,
PUMPHREY R. S. H.,
BOYLSTON A. W.,
OLLLER W. E. R.
Publication year - 1991
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1991.tb05715.x
Subject(s) - immunology , t cell receptor , rheumatoid arthritis , population , human leukocyte antigen , t cell , abnormality , lupus erythematosus , medicine , biology , antigen , antibody , immune system , environmental health , psychiatry
SUMMARY T cell antigen specificity is determined by the products of the genes which encode the variable regions of their receptors. Of the T cell receptor (TCR) variable region gene products examined, only Vβ6.7a TCR‐positive lymphocytes were reduced in primary Sjogren's syndrome patients with IgG 1 hypergammaglobulinaemia compared with an age‐, sex‐ and HLA‐matched control population. The levels of Vβ6.7a T cells were also significantly reduced when these patients were compared with an age‐ and sex‐matched but HLA‐unmatched control group and non‐tissue typed normal people of both sexes. Since published studies show no such abnormality in rheumatoid arthritis, systemic lupus erythematosus or other autoimmune diseases, this abnormality may reflect a pathogenic process specific to primary Sjogren's syndrome.