MicroRNA in TLR signaling and endotoxin tolerance

Nahid, A.; Satoh, Minoru; Chan, Edward K. L.

doi:10.1038/cmi.2011.26

Cited by 269 publications

(251 citation statements)

References 228 publications

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“…Interestingly, miR-146a is a validated modulator of IRAK1 and TRAF6 (Nahid et al 2011), which are key proteins involved in cytokine production (Table 2). Thus, we validated IRAK1 and TRAF6 as protein targets of miR-146a in endothelial cells.…”

Section: Microrna Profile In Replicative Senescence Huvec Cellsmentioning

confidence: 99%

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

Olivieri

Lazzarini

Recchioni

et al. 2012

AGE

184

157

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In order to identify new markers of vascular cell senescence with potential in vivo implications, primary cultured endothelial cells, including human umbilical vein endothelial cells (HUVECs), human aortic endothelial cells (HAECs), human coronary artery endothelial cells (HCAECs) and ex vivo circulating angiogenic cells (CACs), were analysed for microRNA (miR) expression. Among the 367 profiled miRs in HUVECs, miR-146a, miR-9, miR-204 and miR-367 showed the highest up-regulation in senescent cells. Their predicted target genes belong to nine common pathways, including Toll-like receptor signalling (TLR) that plays a pivotal

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Section: Microrna Profile In Replicative Senescence Huvec Cellsmentioning

confidence: 99%

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

Olivieri

Lazzarini

Recchioni

et al. 2012

AGE

184

157

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“…49 Specifically, miR-146 and miR-155 are highly induced within 2 h after TLR treatment, and thus belong to the early-response miRNAs; however, miR-21 belongs to the late-response miRNAs. [52][53][54] There are also subtle differences in miRNA expression profiles depending on the TLR ligands used, stimulation time and specific cell types.…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs in the regulation of TLR and RIG-I pathways

2012

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The innate immune system recognizes invading pathogens through germline-encoded pattern recognition receptors (PRRs), which elicit innate antimicrobial and inflammatory responses and initiate adaptive immunity to control or eliminate infection. Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I) are the key innate immune PRRs and are tightly regulated by elaborate mechanisms to ensure a beneficial outcome in response to foreign invaders. Although much of the focus in the literature has been on the study of protein regulators of inflammation, microRNAs (miRNAs) have emerged as important controllers of certain features of the inflammatory process. Several miRNAs are induced by TLR and RIG-I activation in myeloid cells and act as feedback regulators of TLR and RIG-I signaling. In this review, we comprehensively discuss the recent understanding of how miRNA networks respond to TLR and RIG-I signaling and their role in the initiation and termination of inflammatory responses. Increasing evidence also indicates that both virus-encoded miRNAs and cellular miRNAs have important functions in viral replication and host anti-viral immunity.

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“…In particular, miR-146a is involved in diverse aspects of lymphocyte function, including the modulation of T cell activation (13), Treg suppressor activity (14), and macrophage and DC homeostasis and function (15,16). Previous studies indicate that miR-146a, which expression is predominantly driven by NF-kB, acts as a negative feedback regulator of TLR or retinoic acid-inducible gene signaling pathways by targeting key upstream components, including IL-1R-associated kinase (IRAK) 1, IRAK2, and TNFR-associated factor 6 in macrophages or intestinal epithelial cells (17)(18)(19)(20).…”

mentioning

confidence: 99%

MicroRNA-146a Feedback Suppresses T Cell Immune Function by Targeting Stat1 in Patients with Chronic Hepatitis B

Wang

Zhang

et al. 2013

The Journal of Immunology

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More than 350 million people are chronically infected with hepatitis B virus, and dysfunctional T cell responses contribute to persistent viral infection and immunopathogenesis in chronic hepatitis B (CHB). However, the underlying mechanisms of T cell hyporesponsiveness remain largely undefined. Given the important role of microRNA-146a (miR-146a) in diverse aspects of lymphocyte function, we investigated the potential role and mechanism of miR-146a in regulating T cell immune responses in CHB. We found that miR-146a expression in T cells is significantly upregulated in CHB compared with healthy controls, and miR-146a levels were correlated with serum alanine aminotransaminase levels. Both inflammatory cytokines and viral factors led to miR-146a upregulation in T cells. Stat1 was identified as a miR-146a target that is involved in antiviral cytokine production and the cytotoxicity of CD4+ and CD8+ T cells. In vitro blockage of miR-146a in T cells in CHB greatly enhanced virus-specific T cell activity. Therefore, our work demonstrates that miR-146a upregulation in CHB causes impaired T cell function, which may contribute to immune defects and immunopathogenesis during chronic viral infection.

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MicroRNA in TLR signaling and endotoxin tolerance

Cited by 269 publications

References 228 publications

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

MiR-146a as marker of senescence-associated pro-inflammatory status in cells involved in vascular remodelling

MicroRNAs in the regulation of TLR and RIG-I pathways

MicroRNA-146a Feedback Suppresses T Cell Immune Function by Targeting Stat1 in Patients with Chronic Hepatitis B

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