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Induction and modulation of macrophage Ia antigen expression by platelet‐activating factor
Author(s) -
Erickson Kent L.,
Howard Angela D.,
Hubbard Neil E.
Publication year - 1997
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.62.6.845
Subject(s) - platelet activating factor , biology , inducer , proinflammatory cytokine , macrophage , receptor , microbiology and biotechnology , immunology , endocrinology , inflammation , biochemistry , in vitro , gene
Expression of major histocompatibility complex class II molecules, Ia, can be significantly augmented by interferon‐γ (IFN‐γ) in macrophages. In this study we demonstrate that platelet‐activating factor (PAF) was also a potent inducer of Ia antigen expression on macrophages. PAF‐induced Ia expression was both time‐ and dose‐dependent. Maximal Ia expression was induced with 25 nM PAF after 3‐h exposure to PAF. Ia expression in macrophages stimulated with PAF for 24 h was not significantly greater than unstimulated macrophages. Treatment of macrophages with IFN‐γ and PAF did not affect either the kinetics or concentration required for maximal Ia expression induced by either IFN‐γ or PAF. PAF‐induced Ia expression was inhibited by the specific PAF receptor antagonists, WEB 2086, Ro 24‐0238, and Ro 24‐4637, indicating a receptor‐mediated event Like IFN‐γ‐induced Ia expression, PAF activity was inhibited by prostaglandin E 2 (PGE 2 ). However, that expression was only inhibited after 24 h when macrophages were treated with the PGE 2 synthesis inhibitors, flurbiprofen and indomethacin. These findings demonstrate that PAF, along with its role as a potent proinflammatory mediator, was also capable of inducing Ia expression on macrophages through the PAF receptor and that expression was altered by PGE 2 . J. Leukoc. Biol . 62: 845–851; 1997.