ArticleJournal of the American Society of Nephrology : JASN2008
CXCL9, but not CXCL10, promotes CXCR3-dependent immune-mediated kidney disease.
Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 91 citations in OpenAlex.
- Trial
- Spatial analysis reveals cellular microenvironments and mechanisms of inflammation and injury in acute interstitial nephritis.Nature communications · 2026Article
- Article
- Article
- Identification of Shared Biomarkers and Immune Infiltration Signatures between Vitiligo and Hashimoto's Thyroiditis.Clinical, cosmetic and investigational dermatology · 2024Article
- Proton pump inhibitors and adverse kidney outcomes during immune checkpoint blockade: time to sound the alarm?Clinical kidney journal · 2023Article
- Mesenchymal stem cells enhance CCL8 expression by podocytes in lupus-prone MRL.FasScientific reports · 2023Article
- Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis.The Journal of clinical investigation · 2023Article
- Stress keratin 17 and estrogen support viral persistence and modulate the immune environment during cervicovaginal murine papillomavirus infection.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Glucocorticoids target the CXCL9/CXCL10-CXCR3 axis and confer protection against immune-mediated kidney injury.JCI insight · 2023Article
- Review
- C-X-C Motif Chemokine Ligand 9 and Its CXCR3 Receptor Are the Salt and Pepper for T Cells Trafficking in a Mouse Model of Gaucher Disease.International journal of molecular sciences · 2021Article
- Inhibitory effects of tolerogenic probiotics on migratory potential of lupus patient-derived DCs.Iranian journal of basic medical sciences · 2021Article
- T helper cell trafficking in autoimmune kidney diseases.Cell and tissue research · 2021Review
- Identification of Genes Potentially Associated with Melanoma Tumorigenesis Through Co-Expression Network Analysis.International journal of general medicine · 2021Article
- Acute Kidney Injury in Children after Hematopoietic Cell Transplantation Is Associated with Elevated Urine CXCL10 and CXCL9.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2020Observational
- Renal Fibrosis Is Significantly Attenuated Following Targeted Disruption ofJournal of the American Heart Association · 2020Article
- Type II but Not Type I IFN Signaling Is Indispensable for TLR7-Promoted Development of Autoreactive B Cells and Systemic Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Potential therapeutic manipulations of the CXCR3 chemokine axis for the treatment of inflammatory fibrosing diseases.F1000Research · 2020Article
- Stress keratin 17 enhances papillomavirus infection-induced disease by downregulating T cell recruitment.PLoS pathogens · 2020Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Chemokines are instrumental in macrophage- and T cell-dependent diseases. The chemokine CCL2 promotes kidney disease in two models of immune-mediated nephritis (MRL-Fas(lpr) mice and the nephrotoxic serum nephritis model), but evidence suggests that multiple chemokines are involved. For identification of additional therapeutic targets for immune-mediated nephritis, chemokine ligands and receptors in CCL2-/- and wild-type (WT) MRL-Fas(lpr) kidneys were profiled. The focus was on intrarenal chemokine ligand/receptor pairs that were highly upregulated downstream of CCL2; the chemokine CXCL10 and its cognate receptor, CXCR3, stood out as potential therapeutic targets. However, renal disease was not suppressed in CXCL10-/- MRL-Fas(lpr) mice, and CXCL10-/- C57BL/6 mice were not protected from nephrotoxic serum nephritis compared with WT mice. Because CXCR3 engages with the ligand CXCL9, CXCR3-/- , CXCL9-/- , and CXCL10-/- B6 mice were compared with WT mice with nephrotoxic serum nephritis. Kidney disease, measured by loss of renal function and histopathology, was suppressed in both CXCR3-/- and CXCL9-/- mice but not in CXCL10-/- mice. With nephrotoxic serum nephritis, CXCR3-/- and CXCL9-/- mice had fewer intrarenal activated T cells and activated macrophages. Both IgG glomerular deposits and antigen-specific IgG in serum were reduced in these mice, suggesting that although CXCR3 and CXCL9 initiate nephritis through cell-mediated events, renal inflammation may be sustained by their regulation of IgG. It is concluded that specific blockade of CXCL9
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Registered trials
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