Respiratory syncytial virus infection of human respiratory epithelial cells up-regulates class I MHC expression through the induction of IFN-beta and IL-1 alpha.
Respiratory syncytial virus infection of human respiratory epithelial cells up-regulates class I MHC expression through the induction of IFN-beta and IL-1 alpha.
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DOI：
10.4049/jimmunol.157.6.2506
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发表时间：
1996-09
影响因子：
4.4
通讯作者：
R. Garofalo;Fang C Mei;R. Espejo;Gang Ye;Helene A. Haeberle;Samuel Baron;P. Ogra;Victor E. Reyes
中科院分区：
文献类型：
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作者：
R. Garofalo;Fang C Mei;R. Espejo;Gang Ye;Helene A. Haeberle;Samuel Baron;P. Ogra;Victor E. Reyes
CD 8 + T细胞介导呼吸道合胞病毒（RSV）感染后对肺上皮的一些损伤。由于CD 8 + T细胞识别靶细胞上抗原负载的I类MHC分子，因此我们在本研究中研究了RSV感染的呼吸道上皮细胞I类MHC的表达。呼吸道上皮细胞系和正常人组织的支气管上皮细胞对RSV感染有反应，通过流式细胞术和代谢放射性标记细胞的I类MHC免疫沉淀测定I类MHC表达增加。I类MHC表达的增加依赖于感染性、复制性病毒。当将来自RSV感染的A549细胞的UV照射的培养物上清液添加到新鲜的A549细胞培养物中时，这些细胞诱导I类MHC表达的增加。A549细胞上清液中I类MHC活性的增加在很大程度上是由于IFN-β，在较小程度上是由于IL-1 α。向两种细胞因子中加入中和抗体完全阻断了用上述上清液处理的细胞的I类MHC表达的增加。这些结果表明，RSV感染刺激呼吸道上皮细胞产生IFN-β，这反过来导致它们合成I类MHC的增加，这将促进它们被RSV特异性CD 8 + T细胞识别和裂解。
CD8+ T cells mediate some of the damage to the lung epithelium following respiratory syncytial virus (RSV) infection. Since CD8+ T cells recognize antigen-laden class I MHC molecules on the target cells, we examined in this study the expression of class I MHC by RSV-infected respiratory epithelial cells. Respiratory epithelial cell lines and bronchial epithelial cells from normal human tissue responded to RSV infection with an increased expression of class I MHC as determined by flow cytometry and immunoprecipitation of class I MHC from metabolically radiolabeled cells. The increase in class I MHC expression was dependent on infectious, replicating virus. UV-irradiated culture supernatants from RSV-infected A549 cells, when added to fresh A549 cell cultures, induced an increase in class I MHC expression by those cells. The class I MHC increasing activity within supernatants from A549 cells was due, in large part, to IFN-beta, and to a lesser extent to IL-1 alpha. The addition of neutralizing Abs to both cytokines completely blocked the increase in class I MHC expression by cells treated with the above-mentioned supernatants. These results demonstrate that RSV infection elicits IFN-beta production by respiratory epithelial cells, which in turn leads to an increase in their synthesis of class I MHC, which would facilitate their recognition and lysis by RSV-specific CD8+ T cells.