Abstract

The innate immune response, which is usually referred to as the first line of defense, protects the hosts against pathogenic micro-organisms. Some of the biomolecules released from the pathogens, such as proteins, lipoproteins and nucleic acids, which are collectively termed as pathogen-associated molecular patterns (PAMPs), elicit signaling mechanisms that trigger immune responses in the hosts. Pathogen recognition receptors (PRRs) on the host cells recognize these PAMPs and initiate intracellular signaling through toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and other pathways which induce production of pro-inflammatory cytokines and type I interferons. Recently, different members of tripartite motif containing proteins (TRIM) family of proteins were identified to intercept and regulate these cellular pathways. Specific targets of TRIM proteins have been identified and their molecular mechanisms were unraveled and identified unique domains involved in protein-protein interactions. Though innate immunity represents a tight and well conserved immune system in the host, gene expression in innate immunity was identified to be influenced by several epigenetic mechanisms including regulation by microRNAs (miRNAs). In this review, we present critical analysis of the findings on the identification of specific miRNAs that modulate expression of target genes involved in the regulation of innate immunity.

Highlights

  • The dynamic nature of pathogens, and their ability to invoke modified strategies to escape host immunological recognition, projects challenges in the host to combat invading pathogens

  • Mechanisms underlying the role of suppressor of cytokine signaling protein 1 (SOCS1) in innate immunity appears to be through inhibition of interleukin-1 receptor-associated kinase IRAK1

  • Treatment with IFN-l increases the expression of SOCS3 and the microRNA miR-122 which may have contributed to the inhibition of type I IFN signaling possibly by inducing the gene expression driven by interferon-stimulated response elements (ISRE) [29]

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Summary

Introduction

The dynamic nature of pathogens, and their ability to invoke modified strategies to escape host immunological recognition, projects challenges in the host to combat invading pathogens. C conserved domains of retinoic acid-inducible gene-1 (RIG-I), melanoma differentiation-associated protein 5 (MDA5), Laboratory of genetics and physiology (LGP2) and eIF4A Existence of such a similarity among these proteins suggests that they may have a common regulatory role, and it has been shown that Dicer can potentially interact with RIG-I like receptors [16,17]. These reports unequivocally establish a clear role of Dicer and its chief functions in processing and generating miRNAs regulating innate immunity. We provide published evidence on the identified miRNAs and their characteristic role as epigenetic gene regulators in innate immunity

MicroRNAs Regulate Innate Immune Response
MicroRNAs Inhibit SOCS Proteins in Innate Immunity
Role of miR-223 in Macrophage Polarization
Role of miR-155 in Innate Immunity
Viral microRNAs that Regulate Innate Immunity
RIG-1 and MDA-5 Signaling in Innate Immunity
MicroRNAs Regulate TRIM21-Mediated Innate Immunity
Other Epigenetic Mechanisms Induced by Invading Viruses
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