Interleukin 2 (IL-2) has an important role in the regulation of the expression of IL-2 receptors and the synthesis of gamma interferon (IFN-gamma) by T lymphocytes. IL-2 is required for the optimum expression of IL-2 receptors on activated T lymphocytes and for maximum synthesis of IFN-gamma in vitro. Dexamethasone, an immunosuppressant drug that inhibits IL-2 synthesis, diminished the expression of IL-2 receptors and the synthesis of IFN-gamma. Anti-Tac, a monoclonal antibody known to prevent the binding of IL-2 to its receptor without inhibiting IL-2 synthesis, down-regulated the expression of the receptor and partially inhibited synthesis of IFN-gamma. In a population of T lymphocytes prevented from synthesizing IL-2 by dexamethasone and incapable of using IL-2 as a result of blockage of IL-2 receptors by anti-Tac, the number of receptor-bearing cells and receptor density were diminished. Anti-Tac in combination with dexamethasone also exerted a synergistic effect on IFN-gamma synthesis, inhibiting it almost completely. The inhibitory effect of dexamethasone IFN-gamma synthesis may be of clinical importance, since IFN-gamma activates macrophages and thereby triggers one of the defense mechanisms against bacterial infections.
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Reem et al. (1984) studied this question.
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