Kravis T C, Henson P M
J Immunol. 1977 May;118(5):1569-73.
Circulating 51Cr-labeled platelets accumulate at skin sites in which a reversed passive Arthus reaction has been induced. The accumulation is biphasic in time and is accompanied by an increased vascular permeability. Increased permeability itself, however, will not produce localization of platelets. A similar platelet accumulation was observed upon injection of compound 48/80 or anti-IgE antibody into the skin and this was not altered in rabbits depleted of complement or neutrophils. Activation of skin mast cells and release of a platelet-activating factor (PAF) is suggested as a mechanism for the effect produced by anti-IgE and compound 48/80. The first phase of platelet accumulation in the Arthus reaction was also unaffected in rabbits depleted of neutrophils or complement, which may suggest a role for IgE antibody and mast cells. The second phase of accumulation was diminished in complement-depleted animals and abrogated in rabbits without neutrophils, suggesting a complement and neutrophil-mediated process but which still might be mediated through mast cell activation by neutrophil cationic protein.
循环中的51Cr标记血小板会在已诱导出反向被动Arthus反应的皮肤部位聚集。这种聚集在时间上呈双相性，并伴有血管通透性增加。然而，通透性增加本身并不会导致血小板的定位。将化合物48/80或抗IgE抗体注射到皮肤中时，也观察到了类似的血小板聚集，并且在补体或中性粒细胞耗竭的兔子中这种聚集并未改变。皮肤肥大细胞的激活和血小板激活因子（PAF）的释放被认为是抗IgE和化合物48/80产生作用的一种机制。在中性粒细胞或补体耗竭的兔子中，Arthus反应中血小板聚集的第一阶段也未受影响，这可能提示IgE抗体和肥大细胞的作用。在补体耗竭的动物中，聚集的第二阶段减弱，而在没有中性粒细胞的兔子中则完全消除，这表明这是一个补体和中性粒细胞介导的过程，但仍可能是通过中性粒细胞阳离子蛋白激活肥大细胞来介导的。
