澳大利亞墨爾本大學(xué)微生物學(xué)與免疫學(xué)系一項(xiàng)研究提出,由于參與細(xì)胞介導(dǎo)免疫應(yīng)答的一個(gè)蛋白質(zhì)復(fù)合體的遺傳差異,人們對(duì)2013年2月出現(xiàn)的H7N9流感病毒啟動(dòng)一種細(xì)胞介導(dǎo)免疫的能力可能不同。文章發(fā)表于2014年1月6日的《PNAS》雜志上。
人類此前沒(méi)有遇到過(guò)H7N9病毒,因此缺乏抵抗這種病毒的保護(hù)性抗體。動(dòng)物和人類研究提示,在缺乏抵抗一種新流感毒株的保護(hù)性抗體的情況下,此前產(chǎn)生的抵抗其他流感毒株的交叉反應(yīng)性CD8+ T淋巴細(xì)胞(CTLs)可以減少疾病的嚴(yán)重程度,因此可能提供抵抗H7N9病毒的某些保護(hù)。
Peter Doherty及其同事研究了在此前沒(méi)有接觸過(guò)H7N9病毒的人身上預(yù)先存在的流感特異性交叉反應(yīng)性CD8+ T淋巴細(xì)胞(CTLs)對(duì)H7N9病毒做出應(yīng)答的能力。這組作者發(fā)現(xiàn)有能力引發(fā)交叉反應(yīng)性CD8+ T淋巴細(xì)胞(CTLs)應(yīng)答的28%的H7N9肽也見于導(dǎo)致過(guò)去人類流感大流行或流行的A型流感病毒。這組作者然后估計(jì)有能力把免疫原流感肽呈現(xiàn)給交叉反應(yīng)性CD8+ T淋巴細(xì)胞(CTLs)的人類白細(xì)胞抗原(HLAs)存在于大約16%到57%的人口中,而且依種族的不同,存在率有差異。
研究人員從52名健康人類試驗(yàn)參與者身上得到了血細(xì)胞,并用這些肽在體外培養(yǎng)了血細(xì)胞,其分析結(jié)果表明,某些人類白細(xì)胞抗原(HLAs)等位基因引發(fā)了抵抗包括H7N9在內(nèi)的任何人類A型流感的強(qiáng)烈的交叉反應(yīng)性CD8+ T淋巴細(xì)胞(CTLs)應(yīng)答,而其他一些等位基因,諸如傾向于在阿拉斯加和澳大利亞原住民中間普遍存在的基因,顯示出了有限的交叉反應(yīng)性CD8+ T淋巴細(xì)胞(CTLs)應(yīng)答。這組作者說(shuō),這些發(fā)現(xiàn)提示某些人可能特別容易受到H7N9感染的傷害。
原文摘要:
Preexisting CD8+ T-cell immunity to the novel H7N9 influenza A virus varies across ethnicities
Sergio Quiñones-Parra, Emma Grant, Liyen Loh, Thi H. O. Nguyen, Kristy-Anne Campbell,Steven Y. C. Tong, Adrian Miller, Peter C. Doherty, dhanasekaran Vijaykrishna, Jamie Rossjohn,Stephanie Gras and Katherine Kedzierska
The absence of preexisting neutralizing antibodies specific for the novel A (H7N9) influenza virus indicates a lack of prior human exposure. As influenza A virus–specific CD8+ T lymphocytes (CTLs) can be broadly cross-reactive, we tested whether immunogenic peptides derived from H7N9 might be recognized by memory CTLs established following infection with other influenza strains. Probing across multiple ethnicities, we identified 32 conserved epitopes derived from the nucleoprotein (NP) and matrix-1 (M1) proteins. These NP and M1 peptides are presented by HLAs prevalent in 16–57% of individuals. Remarkably, some HLA alleles (A*0201, A*0301, B*5701, B*1801, and B*0801) elicit robust CTL responses against any human influenza A virus, including H7N9, whereas ethnicities where HLA-A*0101, A*6801, B*1501, and A*2402 are prominent, show limited CTL response profiles. By this criterion, some groups, especially the Alaskan and Australian Indigenous peoples, would be particularly vulnerable to H7N9 infection. This dissection of CTL-mediated immunity to H7N9 thus suggests strategies for both vaccine delivery and development.
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