Yokoyama-Yasunaka J K, Piazza R M, Umezawa E S, Stolf A M
Department of Parasitology, Institute of Ciências Biomédicas, University of São Paulo, Brazil.
J Clin Lab Anal. 1998;12(2):108-14. doi: 10.1002/(SICI)1098-2825(1998)12:2<108::AID-JCLA6>3.0.CO;2-6.
Here, we show that antigal antibodies from Chagas' disease patients react with noninfected host cells previously treated with antigens secreted by the trypomastigote forms of Trypanosoma cruzi. With the exception of human and Old World monkey cells, which are GAL-negative, cells of all mammals express the GAL epitope (Gal alpha (1-3)Gal beta (1-4)GlcNAc-R) on their surface. Thus only the former ones develop antigal antibodies. Antigal antibodies increase during infection with T. cruzi, which expresses GAL epitopes on the surface of the infective forms. Here, we show that incubation of noninfected, GAL-negative cells with antigens shed by T. cruzi renders these cells reactive to antigal antibodies purified from chagasic sera. Neither chagasic sera depleted of antigal antibodies nor antigal antibodies purified from normal sera display reactivity with treated cells. Cell reactivity of chagasic antigal was abolished in the presence of melibiose (Gal alpha (1-6)Glc) or gal-gal (methyl 3-O-alpha-D-galactopyranosyl alpha-D-galactopyranoside). Since shedding of T. cruzi antigens can occur in vivo, these antigens may induce reactivity of chagasic antigal with noninfected human cells. The reactivity of noninfected, GAL-negative cells observed only with chagasic antigal antibodies can amplify the range of reactivity of these antibodies and consequently adds to their importance in the pathogenesis of human Chagas' disease.
在这里,我们发现恰加斯病患者的抗半乳糖抗体与先前用克氏锥虫无鞭毛体形式分泌的抗原处理过的未感染宿主细胞发生反应。除了人类和旧世界猴细胞(它们是半乳糖阴性)外,所有哺乳动物的细胞在其表面都表达半乳糖表位(Galα(1-3)Galβ(1-4)GlcNAc-R)。因此,只有前者会产生抗半乳糖抗体。在感染克氏锥虫期间,抗半乳糖抗体增加,克氏锥虫在感染形式的表面表达半乳糖表位。在这里,我们表明,用克氏锥虫释放的抗原孵育未感染的、半乳糖阴性的细胞,会使这些细胞对从恰加斯病血清中纯化的抗半乳糖抗体产生反应。去除抗半乳糖抗体的恰加斯病血清或从正常血清中纯化的抗半乳糖抗体均未显示与处理过的细胞有反应性。在存在蜜二糖(Galα(1-6)Glc)或半乳糖-半乳糖(甲基3-O-α-D-吡喃半乳糖基-α-D-吡喃半乳糖苷)的情况下,恰加斯病抗半乳糖的细胞反应性被消除。由于克氏锥虫抗原的释放可在体内发生,这些抗原可能诱导恰加斯病抗半乳糖与未感染的人类细胞发生反应。仅用恰加斯病抗半乳糖抗体观察到的未感染的、半乳糖阴性细胞的反应性可扩大这些抗体的反应范围,因此增加了它们在人类恰加斯病发病机制中的重要性。