Abstract
SEVERAL lines of evidence exist implicating prostaglandins (PGs) as mediators in inflammation1. In type IV hypersensitivity (delayed hypersensitivity, cellular immunity) reactions, although there is evidence of PG involvement2,3 lymphokines, the products of antigen-activated thymus-dependent lymphocytes, have received greater attention as potential mediators4,5. It has been reported that PGE1 is a potent inhibitor of lymphocyte activation in vitro6 and we have observed that guinea pig peritoneal exudate macrophages produce substantial amounts of E-type PG (ref. 7). It is well established that macrophages are capable of modifying lymphocyte activation8,9, and that there is close association between these two cell types in reactions of cellular immunity in vitro10 and in vivo11. We have now shown that production of E-type PGs by macrophages modifies the secretion of lymphokines by lymphocytes in response to antigen and that this may serve to provide a negative feedback mechanism for regulating the extent and duration of reactions of cellular immunity.
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GORDON, D., BRAY, M. & MORLEY, J. Control of lymphokine secretion by prostaglandins. Nature 262, 401–402 (1976). https://doi.org/10.1038/262401a0
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DOI: https://doi.org/10.1038/262401a0
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