科學(xué)家在《自然—免疫學(xué)》Nature Immunology上刊文稱,，他們發(fā)現(xiàn)了一些有關(guān)免疫系統(tǒng)是如何識別膜融合—一種發(fā)生在病毒感染細(xì)胞初期的生理過程——的線索,。
研究者發(fā)現(xiàn)，當(dāng)小鼠細(xì)胞暴露在病毒樣顆?；蛘呷鄙龠z傳物質(zhì)和已知刺激分子的人工脂質(zhì)體這兩類物質(zhì)中,，不管是活體實驗還是試管實驗，其仍然可以產(chǎn)生強(qiáng)烈的免疫應(yīng)答,。雖然不能激活任何傳統(tǒng)意義上的病原體識別通路,，但上述兩種物質(zhì)仍可以與細(xì)胞膜融合。
膜融合的識別似乎只能依賴于STING—— 一種細(xì)胞內(nèi)分子,，通常與針對病原體DNA物質(zhì)的應(yīng)答相關(guān),。雖然膜融合自身能產(chǎn)生免疫應(yīng)答，但其也能協(xié)同增強(qiáng)其他免疫刺激信號,，并因此代表了在病原體識別研究中具有普遍意義的重要的第一步,。（生物谷Bioon.com）
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
