关键词： 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

Mesh ： Communicable Diseases / immunology Gene Expression Regulation Humans Immunity, Humoral Immunity, Innate MicroRNAs / metabolism Toll-Like Receptors / immunology metabolism

来  源：   DOI：10.1016/j.jinf.2013.07.016   PDF(Sci-hub)

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.
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