Trial reportMolecular and cellular biochemistry2018
Intrinsic renal cells induce lymphocytosis of Th22 cells from IgA nephropathy patients through B7-CTLA-4 and CCL-CCR pathways.
Trial report in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- CCR1Journal of advanced research · 2026Article
- CCR10: a comprehensive review of its function, phylogeny, role in immune cell trafficking and disease pathogenesis.Frontiers in immunology · 2025Review
- Identification of hub fatty acid metabolism-related genes and immune infiltration in IgA nephropathy.Renal failure · 2024Article
- Molecular Differences in Glomerular Compartment to Distinguish Immunoglobulin A Nephropathy and Lupus Nephritis.Journal of inflammation research · 2024Article
- Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.Frontiers in medicine · 2023Review
- Intratumoral fibrosis and patterns of immune infiltration in clear cell renal cell carcinoma.BMC cancer · 2022Article
- Epigenome-wide association study and network analysis for IgA Nephropathy from CD19Epigenetics · 2021Article
- Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2021Review
- Huangkui Capsule in Combination with Leflunomide Improves Immunoglobulin A Nephropathy by Inhibiting the TGF-β1/Smad3 Signaling Pathway.Clinics (Sao Paulo, Brazil) · 2021Article
- Interleukin-22 attenuates renal tubular cells inflammation and fibrosis induced by TGF-β1 through Notch1 signaling pathway.Renal failure · 2020Article
- Anaphylatoxins enhance Th9 cell recruitment via the CCL20-CCR6 axis in IgA nephropathy.Journal of nephrology · 2020Article
- Gene expression-based analysis identified NTNG1 and HGF as biomarkers for diabetic kidney disease.Medicine · 2020Observational
- 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
- Streptococcus may aggravate inflammatory damage in chronic nephritis via the chemotaxis of Th22 cells.American journal of translational research · 2019Article
- Respiratory Syncytial Virus Exacerbates Kidney Damages in IgA Nephropathy Mice via the C5a-C5aR1 Axis Orchestrating Th17 Cell Responses.Frontiers in cellular and infection microbiology · 2019Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
IgA nephropathy (IgAN), the most common glomerulonephritis, has an unclear pathogenesis. The role of Th22 cells, which are intimately related to proteinuria and progression in IgAN, in mediating infection-related IgAN is unclear. This study aimed to characterize the association between intrinsic renal cells (tubular epithelial cells and mesangial cells) and Th22 cells in immune regulation of infection-related IgAN and to elucidate the impact of Th22 lymphocytosis; the proinflammatory cytokines IL-1, IL-6, and TNF-α; and CCL chemokines on kidney fibrosis. Hemolytic streptococcus infection induced an increase in IL-1, IL-6, and TNF-α, resulting in Th22 cell differentiation from T lymphocytes obtained from patients with IgAN, and the CCL20-CCR6, CCL22-CCR4, and/or CCL27-CCR10 axes facilitated Th22 cell chemotaxis. The increased amount of Th22 cells caused an increase in TGF-β1 levels, and anti-CD80, anti-CD86, and CTLA-4Ig treatment reduced TGF-β1 levels by inhibiting Th22 lymphocytosis and secretion of cytokines and chemokines, thus potentially relieving kidney fibrosis. Our data suggest that Th22 cells might be recruited into the kidneys via the CCL20-CCR6, CCL22-CCR4, and/or CCL27-CCR10 axes by mesangial cells and tubular epithelial cells in infection-related IgAN. Th22 cell overrepresentation was attributed to stimulation of the B7-CTLA-4Ig antigen-presenting pathway and IL-1, IL-6, and TNF-α.
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