Immunological mechanisms of human platelet involvement

Abstract

Several immunological mechanisms of platelet involvement in inflammation are described. Basophils degranulate and release a platelet-activating factor (PAF) when challenged with anaphylotoxins, cationic proteins (CP) from polymorphonuclear cells (PMN) as well as with specific antigens from atopic patients. PAF is a newly-discovered mediator of anaphylaxis present in rabbit and human basophils. This factor is a small phospholipid, probably a lyso-1-phosphatidylcholine with a significant aggregating activity on rabbit and human platelets. PAF is released, together with a small amount of arachidonic acid, from basophils in the presence of anaphylotoxins, CP and specific antigens from atopic patients. The already well-known direct interaction between immune complexes (Ics) and human platelets is compared here with the mechanism of PAF-induced aggregation. It is shown that the latter process of aggregation differs from the former. Human platelet aggregation starts more rapidly in the presence of PAF than of Ics. PAF-induced aggregation is ADP-independent as it is not affected by ADP inhibitors. On the contrary, Ic-dependent aggregation is brought about by endogenous ADP release and therefore inhibited by ADP inhibitors. The interaction between Ics and platelets leads to the release of CP. The latter produce a cascade reaction involving basophils which degranulate and release PAF. A self-maintaining mechanism of tissue injury is thus triggered.