Camussi G, Tetta C, Segoloni G, Vercellone A
Ric Clin Lab. 1978 Oct-Dec;8(4):262-72.
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.
本文描述了血小板参与炎症反应的几种免疫机制。当受到过敏毒素、多形核细胞（PMN）的阳离子蛋白（CP）以及特应性患者的特异性抗原刺激时，嗜碱性粒细胞会脱颗粒并释放血小板激活因子（PAF）。PAF是一种新发现的过敏反应介质，存在于兔和人的嗜碱性粒细胞中。该因子是一种小磷脂，可能是溶血-1-磷脂酰胆碱，对兔和人的血小板具有显著的聚集活性。在过敏毒素、CP和特应性患者的特异性抗原存在的情况下，PAF与少量花生四烯酸一起从嗜碱性粒细胞中释放出来。本文将免疫复合物（Ics）与人类血小板之间早已为人所知的直接相互作用与PAF诱导的聚集机制进行了比较。结果表明，后者的聚集过程与前者不同。在PAF存在的情况下，人类血小板聚集比在Ics存在时开始得更快。PAF诱导的聚集不依赖于ADP，因为它不受ADP抑制剂的影响。相反，Ic依赖性聚集是由内源性ADP释放引起的，因此受到ADP抑制剂的抑制。Ics与血小板之间的相互作用导致CP的释放。后者引发一系列反应，涉及嗜碱性粒细胞脱颗粒并释放PAF。从而触发了一种自我维持的组织损伤机制。
