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抗病毒抗体和补体对病毒感染细胞的损伤机制:IgG、F(ab')2 及替代补体途径的参与

Mechanism of injury of virus-infected cells by antiviral antibody and complement: participation of IgG, F(ab')2, and the alternative complement pathway.

作者信息

Perrin L H, Joseph B S, Cooper N R, Oldstone M B

出版信息

J Exp Med. 1976 May 1;143(5):1027-41. doi: 10.1084/jem.143.5.1027.

Abstract

Antibody-mediated C-dependent lysis of cell lines infected with herpes simplex type 1 virus, influenza A degrees virus, measles virus, and mumps virus occurred by the alternative C pathway with the participation of IgG antibodies. Lysis occurred only with immune human sera, Mg++ EGTA immune sera, and immune sera depleted of C4 or treated with Fab anti-C4. Lysis did not occur with nonimmune sera, Mg++ EDTA immune sera, and immune sera heated 50 degrees C for 25 min, depleted of factor B or treated with Fab antifactor B. Lysis was restored to heated and factor B immunodepleted immune sera by addition of factor B, but not by addition of an excess of C2. Further studies showed that lysis of HeLa cells infected with measles virus was induced by both immune IgG and F(ab')2 but not Fab' in the presence of a nonantibody-containing human C source. Lysis of measles virus-infected cells was also indpendent of movement of viral antigens on the surface of the infected cells, as inhibition of viral antigen capping by cytochalasin B or sodium azide was not associated with abrogation of immune lysis.

摘要

抗体介导的补体依赖性对感染单纯疱疹1型病毒、甲型流感病毒、麻疹病毒及腮腺炎病毒的细胞系的裂解,是通过替代补体途径并在IgG抗体参与下发生的。裂解仅在免疫人血清、含镁离子和乙二醇双四乙酸的免疫血清以及去除C4或用抗C4 Fab处理过的免疫血清中出现。非免疫血清、含镁离子和乙二胺四乙酸的免疫血清以及在50℃加热25分钟、去除B因子或用抗B因子Fab处理过的免疫血清中均未出现裂解。通过添加B因子可使加热及去除B因子的免疫血清恢复裂解能力,但添加过量C2则不能。进一步研究表明,在含非抗体的人补体来源存在时,免疫IgG和F(ab')2均可诱导感染麻疹病毒的HeLa细胞裂解,但Fab'则不能。麻疹病毒感染细胞的裂解也与感染细胞表面病毒抗原的移动无关,因为用细胞松弛素B或叠氮化钠抑制病毒抗原封帽并不伴随免疫裂解的消除。

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