Abstract
Complement-independent chemotactic factor(s) may be generated in fresh guinea pig serum by contact with soluble Ab1Ag1 immune complexes. This activated serum is equally efficient in inducing an unresponsive state in polymorphonuclear neutrophils (PMN) to subsequent chemotaxis challenge with sera containing C-dependent or C-independent chemotactic factors. The unresponsiveness persists long after the removal of serum. Reagents which are inactive on complement but which prevent the generation of C-independent chemotactic factors in fresh serum (diisopropyl fluorophosphate, synthetic esters, kaolin) inhibit both the induction of PMN chemotaxis and the PMN deactivation. Conversely, serum from a guinea pig decomplemented in vivo retains its ability to generate C-independent factors active in PMN attraction and desensitization. The opposition of two pathways for the production of chemotactic factors in serum, one depending on complement, the other on the contact system of coagulation, is again emphasized. A different procedure for inducing unresponsiveness in PMN with soluble complexes in the absence of serum is also presented here.
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