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巨噬细胞获得抗流感病毒活性。

The acquisition of anti-influenza virus activity by macrophages.

作者信息

Mak N K, Ada G L

出版信息

Immunobiology. 1984 May;166(4-5):458-72. doi: 10.1016/S0171-2985(84)80023-6.

Abstract

Exposure of resident peritoneal macrophages or thioglycollate-induced macrophages (TG-Mø) to influenza or Sendai virus-infected spleen cell culture supernatants (MAS) resulted in macrophage activation. When normal resident macrophages were used as effector cells, both infected P815 and L929 cells were lysed in the presence of MAS. MAS-activated TG-Mø also lysed influenza virus-infected L929 cells. Histocompatibility between effector cells and target cells was not required for target cell destruction. The effector cells were plastic-adherent, phagocytic and Ia-. MAS-activated macrophages were also resistant to influenza virus infection in vitro. Both infectious and non-infectious preparations of influenza or Sendai virus preparations were effective at generating MAS. The mediator(s) which renders macrophages to become cytotoxic and resistant to infection was acid-stable, heat-labile (56 degrees C, 30 min; or 100 degrees C, 5 min), and the activity was neutralized by sheep antimouse type 1 interferon (IFN).

摘要

将腹腔常驻巨噬细胞或巯基乙酸盐诱导的巨噬细胞(TG-Mø)暴露于流感病毒或仙台病毒感染的脾细胞培养上清液(MAS)中会导致巨噬细胞活化。当使用正常常驻巨噬细胞作为效应细胞时,在MAS存在的情况下,受感染的P815和L929细胞都会被裂解。MAS激活的TG-Mø也会裂解流感病毒感染的L929细胞。效应细胞与靶细胞之间的组织相容性对于靶细胞的破坏并非必需。效应细胞可黏附于塑料、具有吞噬作用且不表达Ia抗原。MAS激活的巨噬细胞在体外也对流感病毒感染具有抗性。流感病毒或仙台病毒制剂的感染性和非感染性制剂在产生MAS方面均有效。使巨噬细胞具有细胞毒性并对感染产生抗性的介质对酸稳定、对热不稳定(56℃,30分钟;或100℃,5分钟),并且其活性可被羊抗小鼠1型干扰素(IFN)中和。

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