Regulation of polymeric immunoglobulin receptor expression by reovirus
Regulation of polymeric immunoglobulin receptor expression by reovirus
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DOI：
10.1099/vir.0.80690-0
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发表时间：
2005-08-01
影响因子：
3.8
通讯作者：
Cuff, CF
中科院分区：
文献类型：
--
作者：
Pal, K;Kaetzel, CS;Cuff, CF
多聚免疫球蛋白受体（pIgR）从固有层转胞吞二聚伊加和IgA包被的免疫复合物。穿过上皮进入分泌物呼肠孤病毒感染对人肠上皮细胞系HT-29中pIgR表达调节的影响在本报告中进行了表征。在m.o.i.下的复制能力和UV灭活呼肠孤病毒两者。1-100 p.f.u.当量在感染后24小时，每个细胞上调pIgR mRNA，并且在暴露于UV灭活病毒后48小时，细胞内pIgR蛋白增加。需要病毒与HT-29细胞结合，因为将病毒与特异性抗血清（而不是非免疫血清）预孵育可以抑制呼肠孤病毒介导的pIgR上调。导致病毒脱壳的内体酸化是pIglR上调所需的步骤，因为氯化铵或巴弗洛霉素A1预处理抑制病毒诱导的pIgR上调。使用钙蛋白酶抑制剂N-乙酰基-亮氨酰-亮氨酰-正亮氨酸的抑制实验表明，钙蛋白酶参与呼肠孤病毒介导的pIgR上调。病毒感染后pIgR的上调似乎是针对入侵病原体的先天免疫应答，其可以帮助宿主有效地清除感染。由微生物及其产物诱导的信号传导可能有助于增强pIgR介导的伊加转胞吞作用，从而将先天性和获得性免疫应答与病毒联系起来。
Polymeric immunoglobulin receptor (pIgR) transcytoses dimeric IgA and IgA-coated immune complexes from the lamina propria. across epithelia and into secretions. The effect of reovirus infection on regulation of pIgR expression in the human intestinal epithelial cell line HT-29 was characterized in this report. Both replication-competent and UV-inactivated reovirus at m.o.i. equivalents of 1-100 p.f.u. per cell upregulated pIgR mRNA by 24 In post-infection and intracellular pIgR protein was increased at 48 h following exposure to UV-inactivated virus. Binding of virus to HT-29 cells was required, as pre-incubating virus with specific antiserum, but not non-immune serum, inhibited reovirus-mediated pIgR upregulation. Endosomal acidification leading to uncoating of virus is a required step for pIglR upregulation, as ammonium chloride or bafilomycin A1 pre-treatment inhibited virus-induced pIgR upregulation. Inhibition experiments using the calpain inhibitor N-acetyl-leucyl-leucyl-norleucinal suggested that calpains are involved in reovirus-mediated pIgR upregulation. Upregulation of pIgR following virus infection appears to be an innate immune response against invading pathogens that could help the host clear infection effectively. Signalling induced by microbes and their products may serve to augment pIgR-mediated transcytosis of IgA, linking the innate and acquired immune responses to viruses.