ArticleRenal failure2018
Interleukin-17 promotes the production of underglycosylated IgA1 in DAKIKI cells.
Article in Renal failure, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Identification of susceptibility loci and relevant cell type for IgA nephropathy in Han Chinese by integrative genome-wide analysis.Frontiers of medicine · 2024Pooled it
- Renal biopsy findings in psoriasis patients with renal involvement: a descriptive clinicopathologic study.BMC nephrology · 2026Article
- Deciphering the Underlying Mechanisms Linking Psoriasis and IgA Nephropathy.Journal of immunology research · 2026Review
- Advancements in understanding the role of intestinal dysbacteriosis mediated mucosal immunity in IgA nephropathy.BMC nephrology · 2024Review
- Combined Genetic Association and Differed Expression Analysis ofKidney diseases (Basel, Switzerland) · 2024Article
- Sequential administration of paricalcitol followed by IL-17 blockade for progressive refractory IgA nephropathy patients.Scientific reports · 2024Article
- Characterization of T-Cell receptor repertoire in immunoglobulin a nephropathy.Biomarker research · 2024Article
- Pharmacological targets of SGLT2 inhibitors on IgA nephropathy and membranous nephropathy: a mendelian randomization study.Frontiers in pharmacology · 2024Article
- Chemokine (C-C motif) receptor 2 is associated with the pathological grade and inflammatory response in IgAN children.BMC nephrology · 2022Article
- Review
- Association of genetic polymorphisms in IL-23R and IL-17A with the susceptibility to IgA nephropathy in a Chinese Han population.Genes and immunity · 2022Article
- A Functional Variant rs3093023 inFrontiers in immunology · 2021Article
- IgA nephropathy in a patient receiving infliximab for generalized pustular psoriasis.BMC nephrology · 2020Article
- Immunoproteasome in IgA Nephropathy: State-of-Art and Future Perspectives.International journal of biological sciences · 2020Review
- The Role of Immune Modulation in Pathogenesis of IgA Nephropathy.Frontiers in medicine · 2020Review
- T cells in IgA nephropathy: role in pathogenesis, clinical significance and potential therapeutic target.Clinical and experimental nephrology · 2019Review
- Intestinal non-canonical NFκB signaling shapes the local and systemic immune response.Nature communications · 2019Article
- IL-17 in Renal Immunity and Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2018Review
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7 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin 17 (IL-17) plays an important role in the pathogenesis of autoimmune diseases and might be associated with IgA nephropathy (IgAN). This study aimed to investigate the effect of IL-17 on autoimmune pathogenesis in IgA nephropathy.
methodsDAKIKI cells were cultured and stimulated with IL-17 to perform dose-dependent and time-dependent experiments. Cell proliferation was examined by cell counting and the Cell Counting Kit-8 (CCK-8) assay. The IgA concentration and the degree of galactosylation in the supernatant were tested using ELISA and a helix aspersa (HAA) lectin binding assay, respectively. To study the mechanism of O-glycosylation, cells were stimulated with IL-17, lipopolysaccharide (LPS) or 5-azacytidine (5-AZA) + IL-17 for 48 h, and the levels of C1GALT1 and its molecular chaperone Cosmc were measured by western blot and real-time PCR.
resultsThe cell counting and CCK-8 results suggested that B lymphocyte proliferation increased significantly with increased IL-17 concentration. IL-17 affected the quantity of IgA1 and its glycosylation status. HAA revealed that IL-17 promoted IgA1 underglycosylation. Mechanistically, the expression of C1GALT1 and Cosmc was significantly lower in cells stimulated by IL-17 or LPS than in the 5-AZA + IL-17 or the control group.
conclusionsOur results suggested that IL-17 stimulates B lymphocyte to promote B-cell proliferation, which leads to increased IgA1 production in vitro accompanied by underglycosylation of IgA1. The molecular mechanism for the IgA1 underglycosylation induced by IL-17 was similar to that of LPS; however, 5-AZA inhibited IgA1 underglycosylation. IL-17 might participate in IgAN pathogenesis by influencing the production and glycosylation of IgA1 in B-cells.
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