Nat Immun：科学家发现免疫系统对膜融合的识别机制

科学家在《自然—免疫学》Nature Immunology上刊文称，他们发现了一些有关免疫系统是如何识别膜融合—一种发生在病毒感染细胞初期的生理过程——的线索。

研究者发现，当小鼠细胞暴露在病毒样颗粒或者缺少遗传物质和已知刺激分子的人工脂质体这两类物质中，不管是活体实验还是试管实验，其仍然可以产生强烈的免疫应答。虽然不能激活任何传统意义上的病原体识别通路，但上述两种物质仍可以与细胞膜融合。

膜融合的识别似乎只能依赖于STING—— 一种细胞内分子，通常与针对病原体DNA物质的应答相关。虽然膜融合自身能产生免疫应答，但其也能协同增强其他免疫刺激信号，并因此代表了在病原体识别研究中具有普遍意义的重要的第一步。

doi:10.1038/ni.2350
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Virus-cell fusion as a trigger of innate immunity dependent on the adaptor STING

Christian K Holm, Søren B Jensen, Martin R Jakobsen, Natalia Cheshenko, Kristy A Horan, Hanne B Moeller, Regina Gonzalez-Dosal, Simon B Rasmussen, Maria H Christensen, Timur O Yarovinsky, Frazer J Rixon, Betsy C Herold, Katherine A Fitzgerald & Søren R Paludan

The innate immune system senses infection by detecting either evolutionarily conserved molecules essential for the survival of microbes or the abnormal location of molecules. Here we demonstrate the existence of a previously unknown innate detection mechanism induced by fusion between viral envelopes and target cells. Virus-cell fusion specifically stimulated a type I interferon response with expression of interferon-stimulated genes, in vivo recruitment of leukocytes and potentiation of signaling via Toll-like receptor 7 (TLR7) and TLR9. The fusion-dependent response was dependent on the stimulator of interferon genes STING but was independent of DNA, RNA and viral capsid. We suggest that membrane fusion is sensed as a danger signal with potential implications for defense against enveloped viruses and various conditions of giant-cell formation.