Immunoglobulin A (IgA) can inhibit intracellular viral replication during its transport across the epithelial cells. We find a monoclonal IgA antibody 7F1-IgA against the N-terminal moiety of the phosphoprotein (PNT) of measles virus (MV), which inhibits the intracellular replication of MV in Caco-2 cells but not in interferon-deficient Vero-pIgR cells. Transcytosis of 7F1-IgA across the MV-infected Caco-2 cells enhances the production of interferon-β (IFN-β) and the expression of IFN-stimulated genes, rendering Caco-2 cells with higher antiviral immunity. 7F1-IgA specifically interacts with MV phosphoprotein inside the MV-infected Caco-2 cell and prevents MV phosphoprotein from inhibiting the phosphorylation of JAK1 and STAT1. The intraepithelial interaction between 7F1-IgA and the viral phosphoprotein results in an earlier and stronger phosphorylation of JAK1 and STAT1 and, consequently, a more efficient nuclear translocation of STAT1 for the activation of the type I interferon pathway. Thus, IgA against phosphoprotein prevents a virus from evading type I IFN signaling and confers host epithelial cells efficient innate antiviral immunity, which potentiates a new antiviral target and an antiviral strategy.

中文翻译：

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针对病毒磷酸蛋白N端部分的免疫球蛋白A可防止麻疹病毒逃避干扰素-β信号转导。

免疫球蛋白A（IgA）在跨上皮细胞运输过程中可以抑制细胞内病毒复制。我们发现了针对麻疹病毒（MV）磷酸蛋白（PNT）的N末端部分的单克隆IgA抗体7F1-IgA，它抑制了Caco-2细胞中MV的细胞内复制，但没有干扰素缺陷的Vero-pIgR细胞。7F1-IgA跨MV感染的Caco-2细胞的胞吞作用增强了干扰素-β（IFN-β）的产生和IFN刺激基因的表达，使Caco-2细胞具有更高的抗病毒免疫力。7F1-IgA与MV感染的Caco-2细胞内部的MV磷酸蛋白发生特异性相互作用，并阻止MV磷酸蛋白抑制JAK1和STAT1的磷酸化。7F1-IgA与病毒磷蛋白之间的上皮内相互作用导致JAK1和STAT1的磷酸化更早更强，因此，STAT1的核转运更加有效，从而激活了I型干扰素途径。因此，针对磷蛋白的IgA可以防止病毒规避I型IFN信号传导，并赋予宿主上皮细胞有效的先天抗病毒免疫力，从而增强了新的抗病毒靶标和抗病毒策略。