Toll like receptor (TLR)-induced differential expression of microRNAs (MiRs) promotes proper immune response against infections: a systematic review

Abstract

Toll like receptors (TLRs) are one of the major families of pattern recognition receptors (PRRs). MicroRNAs (MiRs) are small noncoding RNAs with regulatory effects on biological process, and it has been recently shown that they can control inflammatory process and the response to an infection by modulating the function of TLRs. In this study, we designed a systematic review to clarify the reciprocal interaction between TLRs and MiRs, in order to identify possible future therapeutic targets and strategies. On the one hand, TLRs stimulation can change expression level of miRs in various ways, which can lead to modulating their effects. On the other hand, MiRs also influence the expression of TLRs and the intensity of the inflammatory reaction. We therefore conclude that the interaction between MiRs and TLRs is a key regulator of innate immune system. Investigations discovering therapeutic approaches by manipulation of miRs expression level may open a new approach for the treatment of inflammatory diseases.

Keywords: C/EBPβ; CCAAT/enhancer-binding protein β; CIS; CaMKII; Calcium/calmodul independent protein kinase II; HIF1-α; IKK; IkappaB kinase. SHIP; Infection; JNK; LPS; MAPK phosphatase-1; MHC II; MKP-1; MicroRNAs; PDCD; Pnak1-α; Programmed Cell Death; SH2-containing inositol phosphatase 1. VSV; SMRT; SOCS4; Suppressor of cytokine signaling; TAB2; TAK1-binding protein 2; TTP; Toll-like receptors; Tristetraprolin; Vesicular somatitis virus; c-Jun N-terminal kinas; cytokine-inducible SH2 protein; hypoxia inducible factor; lipopolysaccharides; major histocompatibility complex class II; mitogen-activated protein kinas p38; p38MAPK; pantothenate kinas 1-α; silencing mediator for retinoid and thyroid hormone receptor.