Tai P C, Spry C J
Clin Exp Immunol. 1980 Apr;40(1):206-19.
Blood eosinophils from some patients with an eosinophilia have a higher capacity to bind to IgC antibody-coated red cells (EA) than blood eosinophils from normal people. Twenty per cent of eosinophils from normal blood bound EA, whereas eight of nine patients with hypereosinophilic syndromes and all nine patients with filariasis who were studied had blood eosinophils with EA rosette-forming capacities of between 42 and 89%. High EA binding capacity was reduced in culture, and prednisolone and cytochalasins A and B inhibited normal blood eosinophil EA binding. Normal blood eosinophils developed small increases in EA binding capacity in culture, but marked increases occurred after stimulation with soluble immune complexes, endotoxins and lipid A. Supernatants from granulocytes cultured with zymosan-C3b caused rapid increases in eosinophils EA binding capacity which also occurred with neuraminidase, pronase and trypsin. In vitro alterations in EA rosetting did not require protein synthesis and did not affect eosinophil phagocytic capacity for EA. Substances in culture which did not affect eosinophil EA rosetting capacity included sera from patients with eosinophils with high EA binding capacity and chemotactic substances. Cultured eosinophils also developed an increased capacity to form rosettes with EAC3b, and soluble immune complexes stimulated this further. Conversely, blood eosinophils formed less C3b rosettes when separated from heparinized blood in which C3 activation had occurred. CytochalasinA (but not B) irreversibly inhibited eosinophils EAC3b rosette formation. Trypsin also inhibited, but this effect was reversed within 30 min after washing. It was concluded that eosinophils from normal blood have an intrinsically lwo capacity to bind EA, but that in vivo and in response to stimulation in vitro their ability to bind complexed IgG can approach that seen with blood neutrophils. It is suggested that enzymes in granulocyte secretion products may cause the membrane changes which lead to high eosinophils EA binding capacity. This increase, which can occur separately from alterations in EAC binding or phagocytic capacity, may enable eosinophils to take part more effectively in inflammatory reactions in tissues.
一些嗜酸性粒细胞增多患者的血液嗜酸性粒细胞与正常人的血液嗜酸性粒细胞相比，具有更高的与IgC抗体包被红细胞（EA）结合的能力。正常血液中20%的嗜酸性粒细胞能结合EA，而在接受研究的9例高嗜酸性粒细胞综合征患者中有8例以及所有9例丝虫病患者的血液嗜酸性粒细胞具有EA花环形成能力，介于42%至89%之间。高EA结合能力在培养中降低，泼尼松龙、细胞松弛素A和B可抑制正常血液嗜酸性粒细胞的EA结合。正常血液嗜酸性粒细胞在培养中EA结合能力有小幅增加，但在用可溶性免疫复合物、内毒素和脂多糖刺激后会有显著增加。用酵母聚糖-C3b培养的粒细胞上清液可使嗜酸性粒细胞的EA结合能力迅速增加，神经氨酸酶、链霉蛋白酶和胰蛋白酶也有此作用。体外EA花环形成的改变不需要蛋白质合成，且不影响嗜酸性粒细胞对EA的吞噬能力。培养中不影响嗜酸性粒细胞EA花环形成能力的物质包括来自具有高EA结合能力嗜酸性粒细胞患者的血清和趋化物质。培养的嗜酸性粒细胞与EAC3b形成花环的能力也有所增加，可溶性免疫复合物可进一步刺激此能力。相反，当从已发生C3激活的肝素化血液中分离时，血液嗜酸性粒细胞形成的C3b花环较少。细胞松弛素A（而非B）可不可逆地抑制嗜酸性粒细胞的EAC3b花环形成。胰蛋白酶也有抑制作用，但洗涤后30分钟内这种作用可逆转。得出的结论是，正常血液中的嗜酸性粒细胞内在结合EA的能力较低，但在体内以及体外受到刺激时，其结合复合IgG的能力可接近血液中性粒细胞的水平。提示粒细胞分泌产物中的酶可能导致膜变化，从而产生高嗜酸性粒细胞EA结合能力。这种增加可独立于EAC结合或吞噬能力的改变而发生，可能使嗜酸性粒细胞更有效地参与组织中的炎症反应。
