Haque A, Ouaissi A, Santoro F, des Moutis I, Capron A
J Immunol. 1982 Nov;129(5):2219-25.
The present study reports the existence of C-mediated adherence of eosinophils and/or macrophages to filarial infective larvae of Dipetalonema viteae. C3 molecules are present on the surface of the parasite, as shown by immunofluorescence studies. Samples of fNRS depleted of AP of complement by treatment with Zymosan A or of factor B by heating at 50 degrees C for 20 min fail to mediate cell adherence to the parasite. In contrast, fNRS inactivated for CP of complement by the chelating agent EGTA retains its activity in mediating cell adherence to the parasite. There is a significant consumption of factor B and AP of complement when infective larvae are incubated in fNHS. Consumption of C4 of the CP of complement is much lower in the same test. The adherence of macrophages cannot occur without the simultaneous presence of eosinophils, whereas eosinophils probably act alone and not in concert with macrophages. The eosinophil adherence is associated with degranulation. The damage is notably enhanced by replacing the spent eosinophil population with a newly obtained population. In the present test system, mast cells did not adhere to filarial larvae even when mast cell-rich populations were used, nor did they effect macrophage adherence when presented in association with the latter. When eosinophil-enriched cell populations containing less than 1% mast cells were used, cell adherence to filarial larvae still occurred, but the presence of 30% mast cells in such cell populations markedly increased both the rate and level of adherence. We suggest that a cell-mediated adherence and destruction dependent upon the activation of complement via AP, without a requirement for specific antibody, may represent a natural mechanism of parasite killing in a nonimmune host.
本研究报告了补体C介导嗜酸性粒细胞和/或巨噬细胞与魏氏棘唇线虫丝状感染性幼虫的黏附现象。免疫荧光研究表明，补体C3分子存在于该寄生虫表面。用酵母聚糖A处理以耗尽补体替代途径（AP）或在50℃加热20分钟以耗尽B因子的新鲜正常兔血清（fNRS）样本，无法介导细胞与寄生虫的黏附。相比之下，用螯合剂乙二醇双四乙酸（EGTA）使补体经典途径（CP）失活的fNRS，在介导细胞与寄生虫的黏附方面仍保留其活性。当感染性幼虫在新鲜正常人类血清（fNHS）中孵育时，补体B因子和AP会有显著消耗。在相同试验中，补体CP的C4消耗要低得多。巨噬细胞的黏附离不开嗜酸性粒细胞的同时存在，而嗜酸性粒细胞可能单独起作用，并非与巨噬细胞协同作用。嗜酸性粒细胞的黏附与脱颗粒有关。用新获得的嗜酸性粒细胞群体替代用过的群体，损伤会显著增强。在本试验系统中，即使使用富含肥大细胞的群体，肥大细胞也不与丝状幼虫黏附，当与巨噬细胞一起呈现时，它们也不影响巨噬细胞的黏附。当使用肥大细胞含量低于1%的富含嗜酸性粒细胞的细胞群体时，细胞仍会与丝状幼虫黏附，但此类细胞群体中30%肥大细胞的存在显著提高了黏附的速率和水平。我们认为，一种依赖于通过AP激活补体的细胞介导的黏附与破坏，无需特异性抗体参与，可能代表了非免疫宿主中杀死寄生虫的一种天然机制。
