ArticlePloS one2017
CCL20 secreted from IgA1-stimulated human mesangial cells recruits inflammatory Th17 cells in IgA nephropathy.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- The chemokine network in lupus nephritis: pathogenesis, targeted therapies, and future directions.Frontiers in pharmacology · 2026Review
- Circulating and Urinary CCL20 in Human Kidney Disease.International journal of molecular sciences · 2025Article
- The immune regulatory role of lymphangiogenesis in kidney disease.Journal of translational medicine · 2024Review
- Semaphorin 5A promotes Th17 differentiation via PI3K-Akt-mTOR in systemic lupus erythematosus.Arthritis research & therapy · 2024Article
- Abatacept Decreases Renal T-cell Infiltration and Renal Inflammation and Ameliorates Progressive Renal Injury in Obese Dahl Salt-sensitive Rats Before Puberty.Journal of cardiovascular pharmacology · 2024Article
- Molecular Differences in Glomerular Compartment to Distinguish Immunoglobulin A Nephropathy and Lupus Nephritis.Journal of inflammation research · 2024Article
- Metformin reduces insulin resistance and attenuates progressive renal injury in prepubertal obese Dahl salt-sensitive rats.American journal of physiology. Renal physiology · 2023Article
- Neutralizing MIP3The Journal of pharmacology and experimental therapeutics · 2023Article
- Interrelation of T cell cytokines and autoantibodies in systemic lupus erythematosus: A cross-sectional study.Clinical immunology (Orlando, Fla.) · 2023Article
- Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.Frontiers in medicine · 2023Review
- T helper 17 cells in the pathophysiology of acute and chronic kidney disease.Kidney research and clinical practice · 2021Article
- Crescentic Glomerulonephritis: Pathogenesis and Therapeutic Potential of Human Amniotic Stem Cells.Frontiers in physiology · 2021Review
- Treatment With Lisinopril Prevents the Early Progression of Glomerular Injury in Obese Dahl Salt-Sensitive Rats Independent of Lowering Arterial Pressure.Frontiers in physiology · 2021Article
- The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis.Frontiers in medicine · 2021Review
- A Functional Variant rs3093023 inFrontiers in immunology · 2021Article
- Anaphylatoxins enhance Th9 cell recruitment via the CCL20-CCR6 axis in IgA nephropathy.Journal of nephrology · 2020Article
- The Role of Immune Modulation in Pathogenesis of IgA Nephropathy.Frontiers in medicine · 2020Review
- Hirudin ameliorates immunoglobulin A nephropathy by inhibition of fibrosis and inflammatory response.Renal failure · 2019Article
- T cells in IgA nephropathy: role in pathogenesis, clinical significance and potential therapeutic target.Clinical and experimental nephrology · 2019Review
- Mesangial Cells Exhibit Features of Antigen-Presenting Cells and Activate CD4+ T Cell Responses.Journal of immunology research · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IgA nephropathy (IgAN) is the most common primary glomerulonephritis characterized by human mesangial cells (HMC) proliferation and extracellular matrix expansion associated with immune deposits consisting of galactose-deficient IgA1. However, how IgA1 contributes to IgAN has yet to be completely elucidated. In this study, the expression profile of chemokines was more altered in IgA1-treated HMC than in the control group. CCL20 was significantly higher either in the serum of IgAN patients or in IgA1-treated HMC. Further experiments demonstrated that CCR6, the only receptor of CCL20, was highly expressed in activated T cells. Intracellular staining assay and cytokine expression profile implied that CCR6+ T cells produced high IL-17 levels. Transwell experiment immunohistochemistry and immunofluorescence experiments extensively demonstrated that CCL20 could recruit inflammatory Th17 cells to the kidneys. These phenomena caused a series of immune inflammatory responses and further damaged the kidneys. Therefore, HMC stimulated by IgA1 could produce CCL20 and consequently recruit inflammatory Th17 cells to the kidneys to induce further lesion in IgA nephropathy.
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