IL-10 alleviates aTCMR by inhibiting NFATc1 signaling pathway of T cells after kidney transplantation

IF 4.2 2区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-21 DOI:10.1016/j.bbadis.2025.167857

Sheng-Li Liu , Peng Zhao , Yan-Man Zhou , Zhi-Guo Peng , Ning Guo , Huai-Bin Sun , Xian-Quan Cui

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引用次数: 0

Abstract

The cause of acute T cell-mediated rejection (aTCMR) is believed to be immune hyperfunction of T cells after kidney transplantation. Nowadays, calcineurin inhibitors are widely used to inhibit the proliferation of T cells when aTCMR occurs. However, the therapeutic dose window of these drugs is relatively narrow and long time use of these drugs may lead to serious side effects. Besides, whether IL-10, a new immune tolerance mediator, playing a therapeutic role on aTCMR remains unclear. The level of IL-10 decreased in patients with aTCMR, suggesting that IL-10 may be involved in the progression of aTCMR. IL-10 could inhibit the proliferation and metabolism of T cells in vitro and in vivo, accompanied by reducing the levels of IL-2, IFN-γ, and TNF-α. Moreover, we confirmed that IL-10 exerts immunosuppressive effects by inhibiting the NFATc1 signaling pathway of T cells. This viewpoint may provide a new therapeutic idea for clinical application.

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IL-10通过抑制肾移植后T细胞的NFATc1信号通路减轻aTCMR

急性T细胞介导的排斥反应（aTCMR）的原因被认为是肾移植后T细胞的免疫功能亢进。目前，钙调磷酸酶抑制剂被广泛用于抑制aTCMR发生时T细胞的增殖。然而，这些药物的治疗剂量窗口较窄，长期使用可能导致严重的副作用。此外，IL-10作为一种新的免疫耐受介质，是否在aTCMR中发挥治疗作用尚不清楚。aTCMR患者IL-10水平下降，提示IL-10可能参与aTCMR的进展。IL-10在体外和体内均能抑制T细胞的增殖和代谢，同时降低IL-2、IFN-γ和TNF-α的水平。此外，我们证实IL-10通过抑制T细胞的NFATc1信号通路发挥免疫抑制作用。这一观点可能为临床应用提供新的治疗思路。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Biochimica et biophysica acta. Molecular basis of disease 生物-生化与分子生物学

CiteScore

12.30

自引率

0.00%

发文量

218

审稿时长

32 days

期刊介绍： BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.