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热灭活流感病毒包被的小鼠靶标的细胞介导裂解

Cell-mediated lysis of heat-inactivated influenza virus-coated murine targets.

作者信息

Hosaka Y, Sasao F, Ohara R

出版信息

Vaccine. 1985 Sep;3(3 Suppl):245-51. doi: 10.1016/0264-410x(85)90116-1.

Abstract

The involvement of inoculated virus antigens in the induction of target susceptibility to cytotoxic T lymphocyte (CTL)-mediated lysis was investigated using heat-inactivated influenza virus, PR8 strain, and various inhibitors in comparison to the cases for live or ultraviolet (u.v.)-irradiated influenza and Sendai viruses. Induction of target susceptibility with heated PR8 was not inhibited by cycloheximide and actinomycin D as in the case of u.v.-irradiated Sendai virus, whereas live virus and u.v.-irradiated PR8 were inhibited under conditions which suppress protein synthesis. Induction of target susceptibility with the live and inactivated PR8 tested was suppressed in the presence of chloroquine, contrary to the case of Sendai virus, and was dependent on the cleavage type of influenza virus haemagglutinin. These findings suggest that the viral target antigens recognized by CTL in heated PR8-coated targets came from inoculated virus proteins, whereas those in PR8-infected or u.v.-irradiated PR8-coated targets involved newly synthesized viral proteins. The former viral target antigens seem to be transferred or processed from the endosome, depending on low pH fusion in the endosomes into which they were engulfed. In this point, the induction of viral target antigens with heated PR8 was different from that induced by u.v.-inactivated Sendai virus. Targets made with heated PR8 were recognized by cross-reactive CTL over the HA subtype.

摘要

使用热灭活的流感病毒PR8株和各种抑制剂,与活的或紫外线(u.v.)照射的流感病毒和仙台病毒的情况相比,研究了接种病毒抗原在诱导靶细胞对细胞毒性T淋巴细胞(CTL)介导的裂解敏感性中的作用。加热后的PR8诱导靶细胞敏感性不受放线菌酮和放线菌素D的抑制,如同紫外线照射的仙台病毒的情况,而活病毒和紫外线照射的PR8在抑制蛋白质合成的条件下则受到抑制。与仙台病毒的情况相反,在所测试的活的和灭活的PR8存在氯喹的情况下,诱导靶细胞敏感性受到抑制,并且这取决于流感病毒血凝素的裂解类型。这些发现表明,CTL在加热的PR8包被的靶细胞中识别的病毒靶抗原来自接种的病毒蛋白,而在PR8感染的或紫外线照射的PR8包被的靶细胞中的那些靶抗原涉及新合成的病毒蛋白。前者的病毒靶抗原似乎是从内体转移或加工而来的,这取决于它们被吞噬进入的内体中的低pH融合。在这一点上,加热的PR8诱导病毒靶抗原的方式不同于紫外线灭活的仙台病毒诱导的方式。用加热的PR8制备的靶细胞被HA亚型上的交叉反应性CTL识别。

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