Purified mouse fibroblast interferon (IF) directly rendered resting macrophages tumoricidal. The physicochemical properties and species specificity of the stimulatory agent fall within the present definition of IF. Since a number of polyanions induce macrophage IF, the antitumor and antimicrobial activities may result from the ability of newly released IF to modify macrophage activity.

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Exogenously added prostaglandins E1 and E2, but not F2alpha, inhibited the tumoricidal activity of interferon-activated macrophages of mice. A role for adenosine 3',5'-monophosphate (cyclic AMP) in modulating macrophage functional activity was suggested because prostaglandins of the E series increase intracellular concentrations of cyclic AMP in macrophages and because treatment of interferon-activated macrophages with dibutyryl cyclic AMP consistently inhibits expression of cytotoxicity. Since the activated macrophage releases high concentrations of prostaglandin E2, it is postulated that this prostaglandin could act locally in negative feedback inhibition to limit cell activities.

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