武漢大學(xué)基礎(chǔ)醫(yī)學(xué)院侯煒教授和武漢大學(xué)動(dòng)物實(shí)驗(yàn)中心科研人員合作的一項(xiàng)科研成果發(fā)表在8月份美國著名國際學(xué)術(shù)刊物《淋巴細(xì)胞生物學(xué)》雜志上,。這項(xiàng)研究發(fā)現(xiàn)，一種名為“表達(dá)CD56分子的T淋巴細(xì)胞”具有抗艾滋病毒感染的作用,。
據(jù)侯煒教授介紹,，這種名為“表達(dá)CD56分子的T淋巴細(xì)胞”是一類“橋梁細(xì)胞”，既具有自然殺傷功能,，又能起到自我保護(hù)作用,。它是人類天然免疫系統(tǒng)的一個(gè)重要的組成部分，在外周血單核細(xì)胞中占5%-15%,，而腸道和肝臟中的50%免疫細(xì)胞為“表達(dá)CD56分子的T淋巴細(xì)胞”,。此前研究只被發(fā)現(xiàn)這種細(xì)胞在抗腫瘤和抗肝炎病毒感染中起作用，而沒有發(fā)現(xiàn)它在抗艾滋病毒感染有較強(qiáng)作用,。
侯煒教授和武漢大學(xué)動(dòng)物實(shí)驗(yàn)中心霍文哲教授團(tuán)隊(duì)歷經(jīng)3年多研究，首次發(fā)現(xiàn)“表達(dá)CD56分子的T淋巴細(xì)胞”培養(yǎng)液中的分泌物可以抑制艾滋病毒的感染和復(fù)制,，并且這種活性具有廣譜性,，既可抑制實(shí)驗(yàn)室保存的艾滋病毒病毒株，也可抑制臨床上分離得到的艾滋病毒病毒株,。
這個(gè)研究團(tuán)隊(duì)發(fā)現(xiàn),，雖然該培養(yǎng)液中的分泌物對(duì)艾滋病毒進(jìn)入細(xì)胞的協(xié)同受體影響甚微，但可增強(qiáng)干擾素調(diào)節(jié)因子的作用,，從而引起巨噬細(xì)胞發(fā)揮作用,，“抗擊”艾滋病毒。（生物谷Bioon.com）
doi: 10.1189/jlb.0312146
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CD56+ T cells inhibit HIV-1 infection of macrophages
Wei Hou, Li Ye and Wen-Zhe Ho
CD56+ T cells, the crucial component of the host innate immune system, play an important role in defense against viral infections. We investigated the noncytolytic anti-HIV-1 activity of primary CD56+ T cells. SNs collected from CD56+ T cell cultures inhibited HIV-1 infection and replication. This CD56+ T SN-mediated anti-HIV-1 activity was broad-spectrum, as CD56+ T SNs could inhibit infections by laboratory-adapted and clinical strains of HIV-1. The antibody to IFN-γ could partially block the CD56+ T SN-mediated anti-HIV effect. Investigation of mechanism(s) of the CD56+ T cell action on HIV-1 showed that although CD56+ T SN had little effect on HIV-1 entry coreceptor CCR5 expression, CD56+ T SN induced the expression of CC-chemokines, the ligands for CCR5. The antibodies to CC-chemokines also significantly blocked CD56+ T SN-mediated anti-HIV activity. Furthermore, CD56+ T SN up-regulated the expression of STAT-1/-2 and enhanced the expression of IRF1, -3, -7, and -9, resulting in the induction of endogenous IFN-α/β expression in macrophages. Moreover, CD56+ T SN up-regulated intracellular expression of APOBEC3G/3F, the recently identified HIV-1 restriction factors. These findings provide compelling evidence that CD56+ T cells may have a critical role in innate immunity against HIV-1 infection.
