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Decreased expression of FcγRIII (CD16) by γδ T cells in patients withrheumatoid arthritis
Author(s) -
Bodmansmith M. D.,
Anand A.,
Durand V.,
Youinou P. Y.,
Lydyard P. M.
Publication year - 2000
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2000.00017.x
Subject(s) - cd16 , fc receptor , synovial fluid , immunology , antigen , antibody , phytohaemagglutinin , rheumatoid arthritis , t cell , immune system , arthritis , medicine , biology , pathology , cd8 , cd3 , osteoarthritis , alternative medicine
Summary Some γδ T cells express a receptor for the Fc portion of immunoglobulin G (FcγRIII – CD16). The relevance of this Fc receptor to γδ T‐cell function is at present unclear. Our previous studies have shown that γδ T cells express activation markers in patients with rheumatoid arthritis (RA). In this study we have examined the relative proportions of CD16 + γδ T cells in the blood and synovial fluid of these patients compared with control blood. CD16 + γδ T cells from RA patients were significantly reduced in synovial fluid compared with the circulation. That this was due to blocking of antibody binding to CD16 was unlikely as treatment of blood γδ T cells with RA synovial fluid (known to contain immune complexes) failed to alter expression of CD16. Treatment of blood γδ T cells with phytohaemagglutinin in vitro , resulted in a time‐dependent decrease in expression of CD16, with a concomitant increase in expression of human leucocyte antigen‐DR, at the single cell level. We conclude that expression of CD16 by γδ T cells is lost in the synovial compartment as the result of activation.