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MicroRNAs: the fine-tuners of Toll-like receptor signalling
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Journal Article
MicroRNAs: the fine-tuners of Toll-like receptor signalling
2011
Overview
Key Points
Multiple microRNAs (miRNAs) are induced by Toll-like receptor (TLR) signalling and regulate the expression of TLR signalling components and TLR-induced cytokines.
TLR-induced miRNAs can influence the innate inflammatory response and have a role in priming of the adaptive immune system.
Notable examples of TLR-induced miRNAs are miR-146a, which targets IL-1R-associated kinase 1 (IRAK1) and TNFR-associated factor 6 (TRAF6); miR-155, which targets the negative regulator Src homology 2 (SH2) domain-containing inositol-5′-phosphatase 1 (SHIP1); and miR-21, which targets the interleukin-10 (IL-10) suppressor molecule programmed cell death 4 (PDCD4).
miRNAs function as fine-tuners of the inflammatory response and have a role in the resolution of inflammation.
Part of the anti-inflammatory effect of IL-10 might be a result of the selective inhibition of miR-155 induced by TLR signalling.
Aberrant expression of TLR-specific miRNAs is associated with inflammatory diseases such as rheumatoid arthritis.
Toll-like receptors (TLRs) are central to the induction of pro-inflammatory responses, but their signalling pathways must be tightly regulated. As discussed in this article, an emerging level of fine-tuning is mediated by microRNAs, several of which are induced by TLR signalling.
Toll-like receptor (TLR) signalling must be tightly regulated to avoid excessive inflammation and to allow for tissue repair and the return to homeostasis after infection and tissue injury. MicroRNAs (miRNAs) have emerged as important controllers of TLR signalling. Several miRNAs are induced by TLR activation in innate immune cells and these and other miRNAs target the 3′ untranslated regions of mRNAs encoding components of the TLR signalling system. miRNAs are also proving to be an important link between the innate and adaptive immune systems, and their dysregulation might have a role in the pathogenesis of inflammatory diseases.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
3' Untranslated Regions - genetics
/ Adaptive Immunity - genetics
/ Animals
/ Biomedical and Life Sciences
/ Cellular signal transduction
/ Gene Expression Regulation - immunology
/ Host-Pathogen Interactions - immunology
/ Humans
/ Proteins
/ RNA, Messenger - biosynthesis
/ Signal Transduction - physiology
/ Toll-Like Receptors - physiology
