T lymphocytes in IgA nephropathy (Review)

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.

The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

“…The Th1 and Th17 immune response mechanisms play a key role in the establishment of productive autoimmune inflammation in the kidneys, as they do in other autoimmune diseases [ 137 , 138 , 139 ]. Damage induced by Th17 manifests itself early, whereas glomerulonephritis caused by Th1 manifests itself later and is characterized by increased macrophage activation and differentiation in the direction of M1.…”

An Update on Targeted Treatment of IgA Nephropathy: An Autoimmune Perspective

“…There is increasing evidence that T cells are associated with the initiation, progression, and disease severity in IgAN. However, the exact mechanisms are not fully understood ( Tang et al, 2020 ). IgAN is characterized by higher proportions of circulatory Th2, Tfh, Th17, Th22, and γδ T-cells and lower proportions of Th1 and Treg cells ( Ruszkowski et al, 2019 ).…”

“…Th1/Th2 imbalance may induce the proliferation of B-lymphocytes and the production of abnormal IgA1 ( Tang et al, 2020 ). Interleukin (IL)-4 (Th2-type), IL-17 (Th17-type), and IL-21 (Tfh-type) are believed to enhance Gd-IgA1 production ( Ruszkowski et al, 2019 ).…”

“…There is increasing evidence that T cells are associated with the initiation, progression, and disease severity in IgAN. However, the exact mechanisms are not fully understood (Tang et al, 2020).…”

Does Th1/Th2 cell imbalance affect immunoglobulin A nephropathy?

“…Th1 lymphocytes contribute to cellular immunity via secretion of interleukin (IL)-2, interferon gamma (IFN-γ), and tumor necrosis factor alpha. Th2 lymphocytes induce humoral immunity by secreting IL-4, IL-5, and IL-13 [ 4 ]. Th1 and Th2 lymphocytes modulate systemic immune system function through mutual regulation ( Fig.…”