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Mechanism of T‐Cell Activation by Mycobacterial Antigens in Inflammatory Synovitis
Author(s) -
BURFORDFOGGS A. M.,
SAMBOL S. P.,
POPE R. M.
Publication year - 1991
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1991.tb01770.x
Subject(s) - synovial fluid , synovitis , immunology , medicine , arthritis , antigen , peripheral blood mononuclear cell , interleukin , rheumatoid arthritis , cytokine , pathology , biology , in vitro , osteoarthritis , biochemistry , alternative medicine
Earlier studies demonstrated enhanced proliferative responses to an acetone precipitable Mycobacterium tuberculosis (AP‐MT) antigenic complex by T lymphocytes from the synovial fluid, compared with the peripheral blood, of patients with inflammatory synovitis. including rheumatoid arthritis. In contrast. decreased proliferation and interleukin 2 (IL‐2) production in response to mitogens by synovial fluid lymphocytes from patients with rheumatoid arthritis has been demonstrated. In order to determine if IL‐2 was produced in response to AP‐MT, the peripheral blood and synovial fluid of patients with inflammatory arthritis were analysed by measuring proliferation and IL‐2 production in response to AP‐MT and tetanus toxoid. A reduction of IL‐2 production relative to proliferation was observed IN some, but not all, synovial fluids of patients who responded to the AP‐MT. Nevertheless, antibodies to IL‐2 as well as interleukin 4 (IL‐4). significantly inhibited proliferation of synovial fluid lymphocytes by AP‐MT. There was no inhibition by antibodies lo interleukin 6 (IL‐6). We conclude that AP‐MT induced proliferation by synovial fluid lymphocytes is mediated by both IL‐2 and lL‐4.