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针对小鼠腺病毒感染的细胞介导免疫。巨噬细胞移动抑制试验。

Cell-mediated immunity to mouse adenovirus infection. Macrophage migration inhibition test.

作者信息

Inada T, Uetake H

出版信息

Microbiol Immunol. 1978;22(7):391-401. doi: 10.1111/j.1348-0421.1978.tb00385.x.

Abstract

Cell-mediated immunity (CMI) to mouse adenovirus (M-Ad) infection was studied by macrophage migration inhibition test (MMI) as one of in vitro correlates of CMI. Both direct and indirect tests showed clearly that migration of packed peritoneal exudate cells (PEC) (immune mouse or nonimmune guinea pig) was remarkably inhibited; MIF was produced by interactions between immune PEC and infected cell extracts and between immune spleen cells and infected cells or their extracts. The antigen(s) responsible for the above MMI was demonstrated in 6- to 12-hour infected ME cells, and FUdR-treated infected ME cells. Since under these conditions there is S antigen(s) synthesis but not capsid antigen synthesis, the antigen(s) concerned must be an S antigen(s). T cells sensitized to infected cells were shown to be required to induce MMI. The MMI is specific for M-Ad, since no cross MMI was observed between M-Ad and SV40 systems. Time course study of the development of CMI to M-Ad by MMI tests showed that CMI became detectable 4 days post-infection (pi), reached its peak level about 10 days pi, and faded away rapidly in about 10 days thereafter.

摘要

通过巨噬细胞迁移抑制试验(MMI)研究了针对小鼠腺病毒(M-Ad)感染的细胞介导免疫(CMI),以此作为CMI的体外相关指标之一。直接试验和间接试验均清楚地表明,聚集的腹膜渗出细胞(PEC)(免疫小鼠或非免疫豚鼠)的迁移受到显著抑制;免疫PEC与感染细胞提取物之间以及免疫脾细胞与感染细胞或其提取物之间的相互作用产生了巨噬细胞移动抑制因子(MIF)。在感染6至12小时的小鼠胚胎(ME)细胞以及经氟尿苷(FUdR)处理的感染ME细胞中,证实了引发上述MMI的抗原。由于在这些条件下有S抗原合成但无衣壳抗原合成,所以相关抗原必定是一种S抗原。结果表明,诱导MMI需要对感染细胞致敏的T细胞。MMI对M-Ad具有特异性,因为在M-Ad和猴空泡病毒40(SV40)系统之间未观察到交叉MMI。通过MMI试验对针对M-Ad的CMI发展进行的时间进程研究表明,感染后4天(pi)可检测到CMI,在感染后约10天达到峰值水平,此后约10天迅速消退。

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