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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)
Publ. Version/Full Text DOI PMC
Open Access Gold (Paid Option)
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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Publication type Article: Journal article
Document type Review
Corresponding Author
Keywords 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
ISSN (print) / ISBN 1534-4827
e-ISSN 1539-0829
Journal Current Diabetes Reports
Quellenangaben Volume: 20, Issue: 9, Pages: , Article Number: 41 Supplement: ,
Publisher Springer
Publishing Place Heidelberg [u.a.]
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Type 1 Diabetes Immunology (TDI)
Grants Projekt DEAL