Role of miRNA-146a in the regulation of the innate immune response and cancer

2008 ◽  
Vol 36 (6) ◽  
pp. 1211-1215 ◽  
Author(s):  
Andrew E. Williams ◽  
Mark M. Perry ◽  
Sterghios A. Moschos ◽  
Hanna M. Larner-Svensson ◽  
Mark A. Lindsay
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Mammalian Cells ◽  
Mrna Translation ◽  
Nuclear Factor Κb ◽  
Causal Link ◽  
Innate Immune ◽  
Major Function ◽  
Biological Responses

In mammalian cells, miRNAs (microRNAs) are the most abundant family of small non-coding RNAs that regulate mRNA translation through the RNA interference pathway. In general, it appears that the major function of miRNAs is in development, differentiation and homoeostasis, which is indicated by studies showing aberrant miRNA expression during the development of cancer. Interestingly, changes in the expression of miR-146a have been implicated in both the development of multiple cancers and in the negative regulation of inflammation induced via the innate immune response. Furthermore, miR-146a expression is driven by the transcription factor NF-κB (nuclear factor κB), which has been implicated as an important causal link between inflammation and carcinogenesis. In the present article, we review the evidence for a role of miR-146a in innate immunity and cancer and assess whether changes in miR-146a might link these two biological responses.

scholarly journals Long Non-Coding RNAs and the Innate Immune Response

2019 ◽  
Vol 5 (2) ◽  
pp. 34 ◽  
Author(s):  
Hadjicharalambous ◽  
Lindsay
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Nuclear Factor Κb ◽  
Innate Immune ◽  
Rapid Induction ◽  
Transcription Process ◽  
Heterogeneous Nuclear Ribonucleoproteins ◽  
In Trans ◽  
Non Coding Rnas

Innate immunity provides the initial defence against infection and it is now clear that long non-coding RNAs (lncRNAs) are important regulators of this response. Following activation of the innate response, we commonly see rapid induction of these lncRNAs and this is often mediated via the pro-inflammatory transcription factor, nuclear factor-κB (NF-κB). Knockdown studies have shown that lncRNAs tend to act in trans to regulate the expression of multiple inflammatory mediators and other responses. Mechanistically, many lncRNAs have demonstrated acting through heterogeneous nuclear ribonucleoproteins, complexes that are implicated chromatin re-modelling, transcription process and translation. In addition, these lncRNAs have also been shown to interact with multiple other proteins involved in the regulation of chromatin re-modelling, as well as those proteins involved in intracellular immune signalling, which include NF-κB. In this review, we will describe the evidence that supports this emerging role of lncRNA in the innate immune response.

scholarly journals The role of beneficial bacteria wall elasticity in regulating innate immune response

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Viktoria V. Мokrozub ◽  
Liudmyla M. Lazarenko ◽  
Liubov M. Sichel ◽  
Lidia P. Babenko ◽  
Petro M. Lytvyn ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Beneficial Bacteria

scholarly journals The transcription factors TFEB and TFE3 link the FLCN-AMPK signaling axis to innate immune response and pathogen resistance

2018 ◽  
Author(s):  
Leeanna El-Houjeiri ◽  
Elite Possik ◽  
Tarika Vijayaraghavan ◽  
Mathieu Paquette ◽  
José A Martina ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Mammalian Cells ◽  
Pathogen Resistance ◽  
Innate Immune ◽  
Negative Regulator ◽  
Energy Status ◽  
Rapid Reduction ◽  
Coupling Energy ◽  
Mtorc1 Signaling

AbstractTFEB and TFE3 are transcriptional regulators of the innate immune response, but the mechanisms regulating their activation upon pathogen infection are poorly elucidated. UsingC. elegansand mammalian models, we report that the master metabolic modulator 5’-AMP-activated protein kinase (AMPK) and its negative regulator Folliculin (FLCN) act upstream of TFEB/TFE3 in the innate immune response, independently of the mTORC1 signaling pathway. In nematodes, loss of FLCN or overexpression of AMPK conferred pathogen resistanceviaactivation of TFEB/TFE3-dependent antimicrobial genes, while ablation of total AMPK activity abolished this phenotype. Similarly, in mammalian cells, loss of FLCN or pharmacological activation of AMPK induced TFEB/TFE3-dependent pro-inflammatory cytokine expression. Importantly, a rapid reduction in cellular ATP levels in murine macrophages was observed upon lipopolysaccharide (LPS) treatment accompanied by an acute AMPK activation and TFEB nuclear localization. These results uncover an ancient, highly conserved and pharmacologically actionable mechanism coupling energy status with innate immunity.

scholarly journals Interferon-Stimulated Genes as Enhancers of Antiviral Innate Immune Signaling

2017 ◽  
Vol 10 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Keaton M. Crosse ◽  
Ebony A. Monson ◽  
Michael R. Beard ◽  
Karla J. Helbig
Keyword(s):  
Immune Response ◽  
Viral Infection ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Regulatory Factor ◽  
Interferon Stimulated Genes ◽  
Innate Immune Signaling ◽  
Recent Advancement ◽  
Antiviral Function

The ability of a host to curb a viral infection is heavily reliant on the effectiveness of an initial antiviral innate immune response, resulting in the upregulation of interferon (IFN) and, subsequently, IFN-stimulated genes (ISGs). ISGs serve to mount an antiviral state within a host cell, and although the specific antiviral function of a number of ISGs has been characterized, the function of many of these ISGs remains to be determined. Recent research has uncovered a novel role for a handful of ISGs, some of them directly induced by IFN regulatory factor 3 in the absence of IFN itself. These ISGs, most with potent antiviral activity, are also able to augment varying arms of the innate immune response to viral infection, thereby strengthening this response. This new understanding of the role of ISGs may, in turn, help the recent advancement of novel therapeutics aiming to augment innate signaling pathways in an attempt to control viral infection and pathogenesis.

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