The functional significance of the regulation of macrophage Ia expression by endogenous arachidonate metabolites in vitro.

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Abstract
We have examined the physiological effects of both exogenously and endogenously produced arachidonic acid metabolites on the expression of class II histocompatibility molecules in murine macrophages. This report shows that both a stable PGI2 analog and PGE2 are effective at suppressing lymphokine-stimulated Ia expression in vitro, whereas indomethacin and ibuprofen potentiate Ia expression, a stable TxA2 analog, TxB2, a thromboxane synthetase inhibitor, and LTC4 were ineffective on lymphokine-induced Ia expression in vitro, the suppression of Ia expression by PGI2 and PGE2 can be partially overcome by increasing the dose of lymphokine, a lymphokine supernatant capable of inducing Ia expression has no effect on the macrophage arachidonate enzyme activities, and the modulation of arachidonate metabolism during macrophage activation occurs differently in vitro than in vivo.