炎性體inflammasome是一組參與先天免疫系統(tǒng)激發(fā)的復(fù)雜蛋白質(zhì),，是大多數(shù)細(xì)胞動(dòng)物的一個(gè)古老的抗菌防衛(wèi)體系。
在4月在線出版的《自然—免疫學(xué)》期刊上,，研究人員報(bào)告了流感病毒激活炎性體的機(jī)制，新發(fā)現(xiàn)也許將有助于科學(xué)家們?cè)O(shè)計(jì)針對(duì)流感病毒應(yīng)激的新防御干涉和治療方式,。
以前的研究發(fā)現(xiàn)，流感病毒M2蛋白質(zhì)是流感病毒致病性的一種重要離子通道,。AkikoIwasaki和同事指出，流感病毒M2蛋白質(zhì)能刺激炎性體通道,。對(duì)炎性體的流感活性來(lái)說(shuō),，M2通道的活性是必要的,。而且，M2對(duì)炎性體活性的調(diào)控需要將之定位在細(xì)胞中細(xì)胞器上的高爾基體上,。
未來(lái)還需要進(jìn)一步的研究,，以求證其他病毒是否也通過(guò)類(lèi)似的離子通道來(lái)激發(fā)炎性體,。(生物谷Bioon.com)
生物谷推薦原文出處：
Nature Immunology (2010) doi:10.1038/ni.1861
Influenza virus activates inflammasomes via its intracellular M2 ion channel
Takeshi Ichinohe, Iris K Pang & Akiko Iwasaki
Influenza virus, a negative-stranded RNA virus that causes severe illness in humans and animals, stimulates the inflammasome through the Nod-like receptor NLRP3. However, the mechanism by which influenza virus activates the NLRP3 inflammasome is unknown. Here we show that the influenza virus M2 protein, a proton-selective ion channel important in viral pathogenesis, stimulates the NLRP3 inflammasome pathway. M2 channel activity was required for the activation of inflammasomes by influenza and was sufficient to activate inflammasomes in primed macrophages and dendritic cells. M2-induced activation of inflammasomes required its localization to the Golgi apparatus and was dependent on the pH gradient. Our results show a mechanism by which influenza virus infection activates inflammasomes and identify the sensing of disturbances in intracellular ionic concentrations as a previously unknown pathogen-recognition pathway.
