4月28日,，美國(guó)《國(guó)家科學(xué)院院刊》(Proceedings of the National Academy of Sciences of the United States of America, 簡(jiǎn)稱PNAS)發(fā)表了武漢大學(xué)生命科學(xué)學(xué)院舒紅兵研究組關(guān)于細(xì)胞抗病毒天然免疫負(fù)反饋調(diào)控機(jī)制的最新研究成果,，論文題目是“ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response”,。該文的第一作者是舒紅兵教授的研究生李穎,，論文中蛋白質(zhì)譜鑒定工作是其與中國(guó)科學(xué)院生物物理所楊福全研究組合作完成的,。
天然免疫是細(xì)胞和機(jī)體天然存在的非特異性或廣譜的抗病原微生物的功能，是機(jī)體抵抗病原微生物的第一道防線,?？共《咎烊幻庖咦钪匾姆绞街皇峭ㄟ^(guò)I型干擾素（α/β干擾素）來(lái)介導(dǎo)的。在過(guò)去幾年中,，舒紅兵研究組發(fā)現(xiàn)了病毒感染誘導(dǎo)I型干擾素表達(dá)的信號(hào)轉(zhuǎn)導(dǎo)中兩個(gè)關(guān)鍵的接頭蛋白VISA和MITA,，論文分別在Molecular Cell和Immunity發(fā)表后，引起廣泛關(guān)注,，其中發(fā)表在Molecular Cell的論文在發(fā)表后三年多時(shí)間里已被SCI他引270多次,。舒紅兵研究組在近年中還發(fā)現(xiàn)了多種抗病毒天然免疫信號(hào)轉(zhuǎn)導(dǎo)的負(fù)調(diào)控機(jī)制，相關(guān)結(jié)果發(fā)表在Immunity, PNAS, EMBO J.等雜志,。
在這項(xiàng)最新研究中,，舒紅兵研究組發(fā)現(xiàn)病毒感染誘導(dǎo)的一個(gè)主要細(xì)胞蛋白ISG56通過(guò)打斷MITA相關(guān)信號(hào)轉(zhuǎn)導(dǎo)復(fù)合物的形成，抑制病毒誘導(dǎo)的I型干擾素表達(dá),，從而揭示了一種新的抗病毒天然免疫信號(hào)轉(zhuǎn)導(dǎo)負(fù)反饋調(diào)控機(jī)制,。該項(xiàng)研究擴(kuò)展了對(duì)ISG56功能機(jī)理的傳統(tǒng)認(rèn)識(shí)，為了解抗病毒天然免疫的精細(xì)調(diào)控機(jī)制提供了新信息,。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS April 28, 2009, doi: 10.1073/pnas.0900818106
ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response
Ying Lia, Chao Lia, Peng Xueb, Bo Zhonga, Ai-Ping Maoa, Yong Rana, He Chena, Yan-Yi Wanga, Fuquan Yangb and Hong-Bing Shua,1
IFN-stimulated gene 56 (ISG56) is one of the first identified proteins induced by viruses and type I IFNs. In this study, we identified ISG56 as a virus-induced protein associated with MITA, an adapter protein involved in virus-triggered induction of type I IFNs. Overexpression of ISG56 inhibited Sendai virus-triggered activation of IRF3, NF-κB, and the IFN-β promoter, whereas knockdown of ISG56 had opposite effects. Consistently, overexpression of ISG56 reversed cytoplasmic poly(I:C)-induced inhibition of vesicular stomatitis virus (VSV) replication, whereas knockdown of ISG56 inhibited VSV replication. Competitive coimmunoprecipitation experiments indicated that ISG56 disrupted the interactions between MITA and VISA or TBK1, two components in the virus-triggered IFN signaling pathways. These results suggest that ISG56 is a mediator of negative-feedback regulation of virus-triggered induction of type I IFNs and cellular antiviral responses.
