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. 2021 Jan 25;8:618536. doi: 10.3389/fcell.2020.618536

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Copyright © 2021 Zhou, Ni, Meng and Tang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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miRNAs regulate T lymphocytes activities to mediate immune and inflammatory processes in DN. During DN progression, miR-155, miR-21, and miR-30b cooperate to promote CD8⁺ T cell activation by repressing SOCS1, DUSP10, and BCL6, respectively. In TIDN, CD3⁺ T cells and pancreas-infiltrating T lymphocytes (PILs) are downregulated by miR-202-3p, which affects the pathogenesis of DN. Moreover, miR155-deficient mice showed a reduced CD4⁺ T cell response to prolong the progression of DN immune disorder. Thus, miRNAs affect DN progression by regulating T lymphocyte-mediated immune functions. BCL6, B-cell chronic lymphocytic leukemia/lymphoma 6; DUSP10, dual specificity phosphatase 10; ICAM-1, intercellular adhesion molecule-1; SOCS1, suppressor of cytokine signaling 1; STAT, signal transducers and activators of transcription; TIDN, type I diabetic nephropathy.