MECHANISMS OF MACROPHAGE ACTIVATION IN RHEUMATOID-ARTHRITIS - THE ROLE OF GAMMA-INTERFERON

  • 1 March 1986
    • journal article
    • research article
    • Vol. 63  (3) , 587-593
Abstract
Gamma-interferon (.gamma.-IFN) is a potent inducer of surface expression of class II MHC molecules in vitro. Enhanced HLA-DR expression is a characteristic immuno-histological feature of rheumatoid joints. To assess the possible relevance of .gamma.-IFN to macrophage (M.vphi.) activation in rheumatoid arthritis (RA) we investigated the spontaneous and mitogen-induced production of .gamma.-IFN by RA lymphocytes using a sensitive radioimmunoassay. Synovial fluids (SF) from a variety of inflammatory and non-inflammatory rheumatic diseases did not contain measurable amounts of IFN. RA lymphocytes from peripheral blood (PBL) and joints failed to show spontaneous .gamma.-IFN production. RA and control PBL were equally responsive to both mitogen stimulation and to the addition of exogenous interleukin 2 (IL-2) as control PBL. SF lymphocytes from RA patients showed a significantly decreased PHA-stimulated .gamma. IFN production and this was in contrast to the SF lymphocytes from patients with other inflammatory joint diseases who showed significantly increased .gamma.-IFN production compared with matched PB lymphocytes. These results show that .gamma.-IFN production by peripheral blood and joint cells from patients with RA is normal and it remains to be established whether .gamma.-IFN is the factor responsible for the macrophage activation seen in the disease.

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