ReviewFrontiers in immunology2026
The role of mucosal immune dysregulation in the pathogenesis of immunoglobulin A nephropathy.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- TLR7/9-mediated mucosal innate immune dysregulation in IgA nephropathy.Frontiers in immunology · 2026Review
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Authors and funding
5 authors.
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Abstract
Immunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide with most patients progressing to kidney failure. Although its pathophysiology remains incompletely understood, deposition of IgA-containing immune complexes in the glomerular mesangium induces mesangial cell proliferation and overproduction of extracellular matrix components and cytokines and chemokines, that lead to glomerular injury. The properties of nephritogenic IgA1 include abnormal glycosylation of its polymeric forms and its capacity to bind IgG autoantibodies to form immune complexes. Nephritogenic IgA1 is thought to be secreted by B cells originating from or residing in mucosa-associated lymphoid tissues (MALT), such as gut-associated lymphoid tissues (GALT) and nasopharynx-associated lymphoid tissues (NALT). However, little is known how the immune abnormalities in MALT elevate the circulatory levels of nephritogenic IgA. This review summarizes fundamental insights into IgA production and its regulation in MALT in general, provides an overview of the immune abnormalities in the MALT of patients with IgAN relevant to the production of abnormally glycosylated IgA, and summarizes relevant emerging treatments tested in clinical trials.
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