Mast cell-mediated microRNA functioning in immune regulation and disease pathophysiology
- PMID: 39812911
- PMCID: PMC11735496
- DOI: 10.1007/s10238-024-01554-2
Mast cell-mediated microRNA functioning in immune regulation and disease pathophysiology
Abstract
Upon stimulation and activation, mast cells (MCs) release soluble mediators, including histamine, proteases, and cytokines. These mediators are often stored within cytoplasmic granules in MCs and may be released in a granulated form. The secretion of cytokines and chemokines occurs within hours following activation, with the potential to result in chronic inflammation. In addition to their role in allergic inflammation, MCs are components of the tumor microenvironment (TME). MicroRNAs (miRNAs) are small RNA molecules that do not encode proteins, but regulate post-transcriptional gene expression by binding to the 3' non-coding regions of mRNAs. This plays a crucial role in the function of MC, including the key processes of MC proliferation, maturation, apoptosis, and activation. It has been demonstrated that miRNAs are also present in extracellular vesicles (EVs) secreted by MCs. EVs derived from MCs mediate intercellular communication by carrying miRNAs, affecting various diseases including allergic diseases, intestinal disorders, neuroinflammation, and tumors. These findings provide important insights into the therapeutic mechanisms and targets of miRNAs in MCs that affect diseases. This review discusses the relevance of miRNA production by MCs in regulating their own activity and the effect of miRNAs putatively produced by other cells in the control of MC activity and their participation in selected pathologies.
Keywords: Disease; EVs; Immune regulation; Mast cell; MicroRNA.
© 2025. The Author(s).
Conflict of interest statement
Declarations. Conflict of Interests: The authors declare no competing interests.
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References
-
- Brzezińska-Błaszczyk E, Bąbolewska E. Stem cell factor-dependent mast cell proliferation maturation and activity can be regulated by inhibitory receptors. Cent Eur J nbsp Immunol. 2013;38(1):134–40.
-
- O’Mahony L, Akdis M, Akdis CA. Regulation of the immune response and inflammation by histamine and histamine receptors. J Allergy Clin Immunol. 2011;128(6):1153–62. - PubMed
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