ArticleJCI insight2023
Glucocorticoids target the CXCL9/CXCL10-CXCR3 axis and confer protection against immune-mediated kidney injury.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Rituximab With or Without Avacopan in ANCA-Associated Vasculitis With Severe Renal Involvement.Kidney international reports · 2026Article
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Immune-Modulatory Mechanism of Compound Yeast Culture in the Liver of Weaned Lambs.Animals : an open access journal from MDPI · 2025Article
- Ras-related protein 2 limits vascular smooth muscle cell phenotypic switching and abdominal aortic aneurysm development.Nature communications · 2025Article
- Identification of circulating immune response-related biomarkers in patients with ANCA-associated glomerulonephritis.Clinical and experimental medicine · 2025Article
- Preconditioning donors with corticosteroids improves early lung graft immunity.Frontiers in immunology · 2025Article
- Investigating interferon type I responses in patients with suspected giant cell arteritis and polymyalgia rheumatica.Clinical and experimental immunology · 2024Article
- The analysis of low-dose glucocorticoid maintenance therapy in patients with primary nephrotic syndrome suffering from COVID-19.Frontiers in molecular biosciences · 2023Article
- Cell-Specific Regulation of Inflammatory Cytokines and Acute-Phase Proteins by the Glucocorticoid Receptor.Mediators of inflammation · 2023Article
- Acute effects of high-dose corticosteroids on serum biomarker profiles in primary CNS demyelinating disease: A pilot study.Multiple sclerosis journal - experimental, translational and clinicalArticle
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Authors and funding
19 authors at 3 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids remain a cornerstone of therapeutic regimes for autoimmune and chronic inflammatory diseases - for example, in different forms of crescentic glomerulonephritis - because of their rapid antiinflammatory effects, low cost, and wide availability. Despite their routine use for decades, the underlying cellular mechanisms by which steroids exert their therapeutic effects need to be fully elucidated. Here, we demonstrate that high-dose steroid treatment rapidly reduced the number of proinflammatory CXCR3+CD4+ T cells in the kidney by combining high-dimensional single-cell and morphological analyses of kidney biopsies from patients with antineutrophil cytoplasmic antibody-associated (ANCA-associated) crescentic glomerulonephritis. Using an experimental model of crescentic glomerulonephritis, we show that the steroid-induced decrease in renal CD4+ T cells is a consequence of reduced T cell recruitment, which is associated with an ameliorated disease course. Mechanistic in vivo and in vitro studies revealed that steroids act directly on renal tissue cells, such as tubular epithelial cells, but not on T cells, which resulted in an abolished renal expression of CXCL9 and CXCL10 as well as in the prevention of CXCR3+CD4+ T cell recruitment to the inflamed kidneys. Thus, we identified the CXCL9/CXCL10-CXCR3 axis as a previously unrecognized cellular and molecular target of glucocorticoids providing protection from immune-mediated pathology.
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