ArticleJournal of the American Society of Nephrology : JASN2015
CXCL5 drives neutrophil recruitment in TH17-mediated GN.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
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- Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of diabetic kidney disease (DKD).Cell death discovery · 2026Review
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- HIV impairs and exploits pulmonary Th17 and Th22 cell-mediated immune responses to Mycobacterium tuberculosis.PLoS pathogens · 2026Article
- Structural dynamics, pathogenic mechanisms, and therapeutic targeting of the NLRP3 inflammasome in lupus nephritis.Frontiers in immunology · 2026Review
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- Novel Tear Biomarkers in Ocular Graft Versus Host Disease Associated with Th1/Th2 Immune Responses: A Case Series and Literature Review.International journal of molecular sciences · 2025Review
- p53: A player in the tumor microenvironment.Oncology research · 2025Review
- Enhancing the treatment potential of IL-17 antagonism in lupus nephritis: finding the right partner.Frontiers in immunology · 2025Review
- Chemokines: humble yet mighty players in the tumour microenvironment.Frontiers in immunology · 2025Review
- The immunoregulatory roles of non-haematopoietic cells in the kidney.Nature reviews. Nephrology · 2024Review
- Human Amniotic MSC Response in LPS-Stimulated Ascites from Patients with Cirrhosis: FOXO1 Gene and Th17 Activation in Enhanced Antibacterial Activation.International journal of molecular sciences · 2024Article
- Chemokine profile in the serum of patients with leptospirosis.Frontiers in cellular and infection microbiology · 2024Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 6 institutions in 2 countries.
Funding
Abstract
Neutrophil trafficking to sites of inflammation is essential for the defense against bacterial and fungal infections, but also contributes to tissue damage in TH17-mediated autoimmunity. This process is regulated by chemokines, which often show an overlapping expression pattern and function in pathogen- and autoimmune-induced inflammatory reactions. Using a murine model of crescentic GN, we show that the pathogenic TH17/IL-17 immune response induces chemokine (C-X-C motif) ligand 5 (CXCL5) expression in kidney tubular cells, which recruits destructive neutrophils that contribute to renal tissue injury. By contrast, CXCL5 was dispensable for neutrophil recruitment and effective bacterial clearance in a murine model of acute bacterial pyelonephritis. In line with these findings, CXCL5 expression was highly upregulated in the kidneys of patients with ANCA-associated crescentic GN as opposed to patients with acute bacterial pyelonephritis. Our data therefore identify CXCL5 as a potential therapeutic target for the restriction of pathogenic neutrophil infiltration in TH17-mediated autoimmune diseases while leaving intact the neutrophil function in protective immunity against invading pathogens.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.