Open AccessHPRT − mutant T cells in the peripheral blood and synovial tissue of patients with rheumatoid arthritis
Author(s) -
Cans Jennifer Leigh,
Karsh Jacob,
Birnboim H. Chaim,
Goldstein Rose
Publication year - 1998
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/1529-0131(199810)41:10<1772::aid-art9>3.0.co;2-c
Subject(s) - rheumatoid arthritis , medicine , immunology , arthritis , pathology , synovial membrane , microbiology and biotechnology , biology
Objective To investigate the frequency and characteristics of hprt ‐ mutant T lymphocytes in the peripheral blood and synovium of rheumatoid arthritis (RA) patients compared with controls, and to correlate these findings with disease parameters. Methods An hprt ‐ T cell assay was performed on blood and synovial samples from 93 RA patients, 8 osteoarthritis (OA) patients, and 19 control subjects. T cell clones were studied by flow cytometry and evaluated for fibronectin adhesion. Results RA patients showed a 5‐fold increase in the frequency of mutant T cells in the peripheral blood compared with that in control peripheral blood, and a further 10‐fold increase in the mutant T cell frequency in synovial tissue. In OA patients, the synovium also had a significantly higher frequency of hprt ‐ mutant T cells compared with the peripheral blood, but at a lower level than in the rheumatoid synovium. RA peripheral blood mutant T cell clones displayed elevated fibronectin adhesion and β1 integrin expression, similar to that observed in the RA synovial T cell lines. Conclusion The origin of the mutated T cells in the peripheral blood of these patients appears to be the inflamed synovium of RA, and to a lesser extent, of OA, where the cells are exposed to a mitogenic and genotoxic environment.