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Scherm, M.G. ; Daniel, C.

miRNA regulation of T cells in islet autoimmunity and type 1 diabetes.

Curr. Diab. Rep. 20:41 (2020)
Verlagsversion DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
Purpose of Review Regulatory T cells (Tregs) are critical contributors to immune homeostasis and their dysregulation can lead to the loss of immune tolerance and autoimmune diseases like type 1 diabetes (T1D). Recent studies have highlighted microRNAs (miRNAs) as important regulators of the immune system, by fine-tuning relevant genes in various immune cell types. In this review article, we discuss recent insights into miRNA regulation of immune tolerance and activation. Specifically, we discuss how the dysregulation of miRNAs in T cells contributes to their aberrant function and the onset of islet autoimmunity, as well as their potential as targets of novel intervention strategies to interfere with autoimmune activation. Recent Findings Several studies have shown that the dysregulation of individual miRNAs in T cells can contribute to impaired immune tolerance, contributing to onset and progression of islet autoimmunity. Importantly, the targeting of these miRNAs, including miR-92a, miR-142-3p and miR-181a, resulted in relevant effects on downstream pathways, improved Treg function and reduced islet autoimmunity in murine models. miRNAs are critical regulators of immune homeostasis and the dysregulation of individual miRNAs in T cells contributes to aberrant T cell function and autoimmunity. The specific targeting of individual miRNAs could improve Treg homeostasis and therefore limit overshooting T cell activation and islet autoimmunity.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Immune Regulation ; Islet Autoimmunity ; Type 1 Diabetes ; Regulatory T Cell ; Mirna ; Biomarker; Blood Mononuclear-cells; Decreased Expression; Immune Dysregulation; Foxp3 Demethylation; Mir-155 Contributes; Micrornas; Targets; Beta; Differentiation; Autoantigen
Sprache
Veröffentlichungsjahr 2020
HGF-Berichtsjahr 2020
ISSN (print) / ISBN 1534-4827
e-ISSN 1539-0829
Zeitschrift Current Diabetes Reports
Quellenangaben Band: 20, Heft: 9, Seiten: , Artikelnummer: 41 Supplement: ,
Verlag Springer
Verlagsort Heidelberg [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit Type 1 Diabetes Immunology (TDI)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502191-001
Förderungen Projekt DEAL
DOI 10.1007/s11892-020-01325-9
WOS ID WOS:000556695900002
Scopus ID 85088635264
PubMed ID 32725277
Erfassungsdatum 2020-10-05
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