Decreased expression of FcgammaRIII (CD16) by gammadelta T cells in patients with rheumatoid arthritis

• Published in: Immunology 2000-04, Vol.99 (4), p.498-503
• Main Authors: Bodman-Smith, M D, Anand, A, Durand, V, Youinou, P Y, Lydyard, P M
• Format: Article
• Language: English
• Subjects: Arthritis, Rheumatoid - immunology; Biomarkers - analysis; Case-Control Studies; Cells, Cultured; HLA-DR Antigens - analysis; Humans; Lupus Erythematosus, Systemic - immunology; Lymphocyte Activation - drug effects; Phytohemagglutinins - pharmacology; Receptors, Antigen, T-Cell, gamma-delta - immunology; Receptors, IgG - analysis; Statistics, Nonparametric; Synovial Fluid - immunology; T-Lymphocytes - immunology; Time Factors
• ISSN: 0019-2805

Some gammadelta T cells express a receptor for the Fc portion of immunoglobulin G (FcgammaRIII - CD16). The relevance of this Fc receptor to gammadelta T-cell function is at present unclear. Our previous studies have shown that gammadelta T cells express activation markers in patients with rheumatoid arthritis (RA). In this study we have examined the relative proportions of CD16+ gammadelta T cells in the blood and synovial fluid of these patients compared with control blood. CD16+ gammadelta 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 gammadelta T cells with RA synovial fluid (known to contain immune complexes) failed to alter expression of CD16. Treatment of blood gammadelta 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 gammadelta T cells is lost in the synovial compartment as the result of activation.