Abstract

Allergic inflammation is accompanied by the coordinated expression of numerous genes and proteins that initiate, sustain, and propagate immune responses and tissue remodeling. MicroRNAs (miRNAs) are a large class of small regulatory molecules that are able to control the translation of target mRNAs and consequently regulate various biological processes at the posttranscriptional level. MiRNA profiles have been identified in multiple allergic inflammatory diseases and in the tumor microenvironment. Mast cells have been found to co-localize within the above conditions. More specifically, in addition to being essential in initiating the allergic response, mast cells play a key role in both innate and adaptive immunity as well as in modulating tumor growth. This review summarizes the possible role of various miRNAs in the above-mentioned processes wherein mast cells have been found to be involved. Understanding the role of miRNAs in mast cell activation and function may serve as an important tool in developing diagnostic as well as therapeutic approaches in mast cell-dependent pathological conditions.

Highlights

  • MicroRNAs are a class of short single-stranded RNA molecules that are only 19 to 25 nucleotides long that serve as negative regulators of protein expression

  • Toll-like receptors (TLRs), some polybasic compounds known as microvesicles derived from activated T cells can stimulate Mast cells (MC) to degranulate and release basic secretagogues, peptides, dextran, complement, IgG-antigen complexes, proteases, cytokines, and several cytokines that are specific to this activation pathway, such as IL‐24 and chemokines, endogenous mediators within the nervous system such as neurotensin and somatostatin

  • We have previously shown that microvesicles derived from activated T cells can stimulate MC to degranulate and release several cytokines that are specific to this activation pathway, such as IL-24 and Oncostatin M (OSM) [22]

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Summary

Introduction

MicroRNAs (miRNAs) are a class of short single-stranded RNA molecules that are only 19 to 25 nucleotides long that serve as negative regulators of protein expression. The interaction of IgE with its receptor results in the phosphorylation variety of bioactive mediators that are pre-stored in cytoplasmic granules, including histamine, heparin, of spleen tyrosine kinase (Syk), calcium (Ca2+) influx, and the activation of protein kinase C (PKC), proteases, proteoglycan, and antimicrobial are factor rapidly(NF‐κB). As IgE basic secretagogues, peptides dextran, complement,ofIgG‐antigen complexes, proteases, cytokines, influx, and the activation of protein kinase Cwithin (PKC),the mitogen-activated (MAPK), and and chemokines, endogenous mediators nervous systemprotein such kinase as neurotensin and nuclear factor (NF-κB). Toll-like receptors (TLRs), some polybasic compounds known as microvesicles derived from activated T cells (mvT*) can stimulate MC to degranulate and release basic secretagogues, peptides, dextran, complement, IgG-antigen complexes, proteases, cytokines, and several cytokines that are specific to this activation pathway, such as IL‐24 and Oncostatin. This review will focus on recent findings that are relevant to the effect of miRNA on MC function in both allergic and non-allergic immune responses

Expression of miRNAs in MC
Involvement of miRNAs in IgE-Mediated Allergic Diseases
Involvement of miRNAs in Non-Allergic Diseases
MiRNAs Involvement in MC–Tumor Interaction
Concluding Remarks
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