Abstract
A dissociation between the in situ generation of lymphocyte-dependent macrophage chemotactic activity (MCA) and the accumulation of macrophages in peritoneal inflammatory exudates was demonstrated in rats stimulated intraperitoneally with a saline suspension of killed Listeria monocytogenes (LM). Treatment of specifically immunized animals with cobra venom factor (CoVF) erased the hemolytic activity of serum complement (C) and the generation of peritoneal MCA. Such C-deficient rats nonetheless marshaled a substantial number of monocyte-derived macrophages into LM-induced exudates. The results suggest that MCA does not have an obligatory role in the attraction of macrophages into lesions in which there is a delayed inflammatory component. CoVF not only abrogated lymphocyte-dependent MCA in antigen-induced exudates but also decreased MCA of fresh and of heated normal rat serum. The serum of venom-treated animals could not be rendered chemotactic by C activation. It remains to be determined whether lymphocyte-dependent MCA is a product of antigen-stimulated T cells or is generated extracellularly by the interaction of T-cell factors with a humoral precursor. In any event, lymphocyte-dependent MCA differs from C-dependent MCA insofar as it is inactivated by heating (30 min at 56 °C).
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