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. 2016 Dec 5;7:563. doi: 10.3389/fimmu.2016.00563

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Copyright © 2016 Villena, Vizoso-Pinto and Kitazawa.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Innate immune response against rotavirus in intestinal epithelial cells (IECs). Rotavirus double-strand genomic RNA activates toll-like receptor 3 (TLR3), retinoic acid-inducible gene-I (RIG-I), and melanoma differentiation-associated gene-5 (MDA-5), which are pattern recognition receptors (PRRs) expressed in IECs. Cellular signaling cascades are activated and converge at the level of interferon (IFN) regulatory factor-3 (IRF3) that upregulate the expression of type I (IFN-α, IFN-β) and type III (IFNλ1, IFNλ2/3) IFN, which in turn induces the synthesis of IFN-stimulated genes with antiviral activities (MxA, Mx1, RNase L, OAS, PKR). Antiviral PRRs also activate nuclear factor κB (NF-κB) pathway and induce the secretion of proinflammatory cytokines and chemokines (IL-6, IL-8, MCP-1, CXCL10). Those effects could be imitated in vitro and in vivo by administration of the dsRNA synthetic analog poly(I:C).