MicroRNA-466l Upregulates IL-10 Expression in TLR-Triggered Macrophages by Antagonizing RNA-Binding Protein Tristetraprolin-Mediated IL-10 mRNA Degradation

Ma, Feng; Liu, Xingguang; Liu, Dong; Wang, Pin; Li, Nan; Lu, Liwei; Cao, Xuetao

doi:10.4049/jimmunol.0902308

Cited by 221 publications

(187 citation statements)

References 43 publications

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“…A previous study has also shown that miR-466l enhances the production of immune-suppressive IL-10. 26 Thus, enhancing the expression or activity of miR-466l may be a new approach for both the prevention of virusinduced cytokine storms and the treatment of autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

“…A previous report has suggested that miR-466l could bind to the ARE of IL-10 39UTR, thereby upregulating IL-10 expression by antagonizing RNA-binding protein tristetraprolin-mediated IL-10 mRNA degradation. 26 Whether miR-466l can regulate host antiviral innate immune response, specifically type I IFN production, remains unknown. In this study, we focused on the role of miR-466l in this process.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-466l inhibits antiviral innate immune response by targeting interferon-alpha

Fan

et al. 2012

Cell Mol Immunol

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Effective recognition of viral infections and subsequent triggering of antiviral innate immune responses are essential for the host antiviral defense, which is tightly regulated by multiple regulators, including microRNAs (miRNAs). A previous study showed that miR-466l upregulates IL-10 expression in macrophages by antagonizing RNA-binding protein tristetraprolin-mediated IL-10 mRNA degradation. However, the ability of miR-466l to regulate antiviral immune responses remains unknown. Here, we found that interferon-alpha (IFN-a) expression was repressed in Sendai virus (SeV)-and vesicular stomatitis virus (VSV)-infected macrophages and in dendritic cells transfected with miR-466l expression. Moreover, multiple IFN-a species can be directly targeted by miR-466l through their 39 untranslated region (39UTR). This study has demonstrated that miR-466l could directly target IFN-a expression to inhibit host antiviral innate immune response.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-466l inhibits antiviral innate immune response by targeting interferon-alpha

Fan

et al. 2012

Cell Mol Immunol

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“…For example, the seed sequence of miR-466l is complementary to the AU-rich element sequence 'AUUUA' of Il-10 mRNA and, thus, can compete with tristetraprolin for the AU-rich element sequence binding, resulting in elevated IL-10 production from macrophages. 107 Thus, it is interesting to identify miRNAs involved in the direct mRNA regulation of TLR-induced cytokine expression.…”

Section: Mirnas In Regulation Of Tlr and Rig-i Pathways Yk LI And Xy mentioning

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 other word, deregulated expression of these miRNAs represents an underlying trigger inducing LN and its pathogenesis (14). Some of these miRNAs directly involve in expression of pro-inflammatory cytokines that dictate magnitude of immune response (15)(16)(17). Within the recent two decades, more than 140 conserved miRNAs were discovered that have specific target site on 72 candidate genes for lupus and LN (18).…”

Section: Discussionmentioning

confidence: 99%

Assessment of microRNA profile of kidney biopsies of patients with lupus nephritis

Malakoutian¹,

Hajian²,

Ebrahimi³

et al. 2017

J Nephropathol

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Background: The changes in some epigenetic elements such as microRNAs result in aberrant immune responses leading to production and secretion of nephritogenic autoantibodies as the main fundament of lupus nephritis (LN).Objectives: The present study aimed to assess the miRNA profile of kidney biopsies in patients with LN with the purpose of describing the critical role of these elements in LN creation. Patients and Methods:In this case-control single center study 11 patients who suffered LN (as the case group) and 11 patients with normal kidney function who were candidate for nephrectomy due to cancer or cyst (as the control group) were included. Kidney biopsies were taken from all LN and control subjects. RNA was extracted and converted to cDNA, then the cDNA was evaluated using NANODROP and then intra-renal expression of candidate miRNAs were quantified in the two groups. In the present study, four topranked miRNAs, miR-638, miR-146a, miR-198, and miR-731 were selected for qRT-PCR. Results: Consistent with the microarray data, we found no significant difference in the expression of all miRNAs between LN and control groups. Using REST 2009 software, we did not also reveal any difference in expression of four miRNAs studied between the patients with LN and those without LN in both parametric and nonparametric patterns. Conclusions:The expression of miR-638, miR-146a, miR-198, and miR-731 may not be related to occurrence of LN in Iranian population.

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MicroRNA-466l Upregulates IL-10 Expression in TLR-Triggered Macrophages by Antagonizing RNA-Binding Protein Tristetraprolin-Mediated IL-10 mRNA Degradation

Abstract: Material

Cited by 221 publications

References 43 publications

MicroRNA-466l inhibits antiviral innate immune response by targeting interferon-alpha

MicroRNA-466l inhibits antiviral innate immune response by targeting interferon-alpha

MicroRNAs in the regulation of TLR and RIG-I pathways

Assessment of microRNA profile of kidney biopsies of patients with lupus nephritis

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