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. 2020 Apr 22;20(1):186–194. doi: 10.3892/etm.2020.8673

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Copyright: © Tang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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T cells in the pathogenesis of IgA nephropathy. IgA nephropathy (IgAN) is characterized by the accumulation of immune complexes in the circulation. It is mainly composed of galactose-deficient IgA1 (Gd-IgA 1) and Gd-IgA1 deposition in the renal mesangium, causing local proliferation and matrix expansion. Gd-IgA1 has been confirmed as one of the key effectors in the pathogenesis of IgAN. Recent studies have shown that T lymphocytes play a crucial role in the development of IgAN. T-cell dysregulation may induce B cells to secrete excessive and abnormal IgA1, leading to IgA deposition in the glomerulus and injury. Stat, signal transducer and activator of transcription; IL, interleukin; Tfh, follicular helper T cell; Th, helper T cell; IFN, interferon; TNFα, tumor necrosis factor α; TGF-β, transforming growth factor β.