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

T lymphocytes in IgA nephropathy

Yuyan Tang  1 , Haidong He  1 , Pin Hu  1 , Xudong Xu  1
Affiliations

T lymphocytes in IgA nephropathy

Yuyan Tang et al. Exp Ther Med. 2020 Jul.

Abstract

Immunoglobulin A nephropathy (IgAN), the most common primary glomerulonephritis worldwide, is the main cause of end-stage renal disease. IgAN is characterized by the accumulation of immune complexes in the circulation, which contain abnormal levels of IgA. IgAN primarily results from galactose-deficient IgA1 (Gd-IgA1) 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, but the origin of Gd-IgA1 is not clear. Recent studies have shown that Gd-IgA1 deposition could be the result of mucosally primed plasma cells and is associated with T cell dysregulation. T cells contribute to the IgA response and play an important role in the development of IgAN. In the present review, the latest discoveries regarding the role of T lymphocytes in the pathogenesis of IgAN have been summarized. Understanding these advances will allow novel therapeutic strategies for the treatment of IgAN.

Keywords: B lymphocyte; IgA nephropathy; T lymphocyte; galactose-deficient IgA1; pathogenesis.

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Figures

Figure 1
Figure 1
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.
See this image and copyright information in PMC

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