在微小病毒科中，小兒麻痺病毒及克沙奇B3病毒都存在著干擾宿主免疫反應的機制: 負調控宿主表面第一型組織相容性複合物(MHC class I)的表現及其調控的細胞免疫反應。而我們的研究即是想探討腸病毒71型(EV71)是否也存在著類似的機制。我們觀察人類胚胎橫紋肌肉瘤細胞(RD)、人類結腸腺癌(Caco-2)、人類神經細胞瘤(SK-N-SH)、小鼠神經細胞瘤(Neuro-2a)、小鼠巨噬細胞(RAW264.7)在與不同劑量的EV71、不同時間共同培養後的感染狀況以及細胞表面MHC class I之表現量，結果發現，EV71感染RD、Caco-2、SK-N-SH及Neuro-2a後皆會造成MHC class I之負調控，我們更進一步發現表現VP1或2C病毒蛋白的RD細胞亦有相同結果且屬於轉譯後的機制。此外，表現2C病毒蛋白的RD細胞與空白載體及表現VP1的細胞比較後，發現其降低了活化異種淋巴球的效果。以上結果顯示，EV71感染後造成宿主細胞表面MHC class I負調控可能會減少MHC class I所媒介的細胞免疫反應，很可能是EV71逃脫細胞免疫的策略。

In this study, we sought to test whether or not enterovirus 71 (EV71) could down-regulate the expression of major histocompatibility complex class I molecule (MHC class I) of host cells, a well-known immune escape mechanism exerted by other members of the Family Picornaviridae, including poliovirus and coxsackie B3 virus. Specifically, we monitored the expression of MHC class I molecule on human rhabdomyosarcoma (RD), colorectal adenocarcinoma (Caco-2), and neuroblastoma (SK-N-SH), and mouse neuroblastoma (Neuro-2a) and monocyte (RAW264.7) by flow cytometry after incubation of the cells with EV71. Our data indicated that EV71 down-regulated MHC class I expression on the surface of RD, Caco-2, SK-N-SH and Neuro-2a cells in a post-translational mechanism. Similar results were also observed in cells transfected with the plasmids expressing either the VP1 or 2C gene of EV71. The 2C protein expressing RD cells with a reduced expression of MHC class I induced a lower proliferation of xenogenic lymphocytes than cells expressing blank plasmid or the VP1. These results illustrated that EV71-infected cells might become less sensitive to cellular immunity as a result of reduced expression of surface MHC class I. These effects may represent an important mechanism for immune evasion of EV71.

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