ArticleJournal of the American Society of Nephrology : JASN2016
CXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 82 citations in OpenAlex.
- A novel CAF population coordinates hyper-suppressive regulatory T cell recruitment and localization in lung cancer.Nature immunology · 2026Article
- Targeting FOXP3 and Regulatory T Cells in Systemic Lupus Erythematosus: Emerging Therapeutic Strategies and Clinical Prospects.Journal of cellular biochemistry · 2026Review
- IL-2 mutein promotes antigen-specific transplant acceptance in mice through expansion of ST2Nature communications · 2026Article
- Treg-derived IFN-γ supports the differentiation of Th1-Treg in tumor immunity and autoimmunity.Frontiers in immunology · 2026Article
- Decoding Treg diversity and dysfunction to advance Treg-based therapies in autoimmune and inflammatory diseases.Frontiers in immunology · 2026Review
- CXCR3 ameliorates neutrophil-dependent disease severity in SARS-CoV-2 infection by regulating CD4Frontiers in immunology · 2026Article
- Ocular immune privilege in action: The living eye imposes unique regulatory and anergic gene signatures on uveitogenic T cells.Cell reports · 2025Article
- Cxcr3 promotes protection from colorectal cancer liver metastasis by driving NK cell infiltration and plasticity.The Journal of clinical investigation · 2025Article
- Development of DPP-4-resistant CXCL9-Fc and CXCL10-Fc chemokines for effective cancer immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Chemokines Signature and T Cell Dynamics in Leishmaniasis: Molecular insight and therapeutic application.Expert reviews in molecular medicine · 2024Review
- PD-1 and CTLA-4 serve as major gatekeepers for effector and cytotoxic T-cell potentiation by limiting a CXCL9/10-CXCR3-IFNγ positive feedback loop.Frontiers in immunology · 2024Article
- Regulation of Treg cells by cytokine signaling and co-stimulatory molecules.Frontiers in immunology · 2024Review
- Deciphering the developmental trajectory of tissue-resident Foxp3Frontiers in immunology · 2024Review
- Chemokines and Cytokines Profiles in Patients with Antineutrophil Cytoplasmic Antibodies-Associated Vasculitis: A Preliminary Study.International journal of molecular sciences · 2023Article
- CXCR3 expression in regulatory T cells drives interactions with type I dendritic cells in tumors to restrict CD8Immunity · 2023Article
- TCF-1 negatively regulates the suppressive ability of canonical and noncanonical Tregs.Journal of leukocyte biology · 2023Article
- Glucocorticoids target the CXCL9/CXCL10-CXCR3 axis and confer protection against immune-mediated kidney injury.JCI insight · 2023Article
- Chronic CD27-CD70 costimulation promotes type 1-specific polarization of effector Tregs.Frontiers in immunology · 2023Article
- Coexpression of PD-L1/PD-1 with CXCR3/CD36 and IL-19 Increase in Extranodal Lymphoma.Journal of immunology research · 2023Article
- Review
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemokines and chemokine receptors are implicated in regulatory T cell (Treg) trafficking to sites of inflammation and suppression of excessive immune responses in inflammatory and autoimmune diseases; however, the specific requirements for Treg migration into the inflamed organs and the positioning of these cells within the tissue are incompletely understood. Here, we report that Tregs expressing the TH1-associated chemokine receptor CXCR3 are enriched in the kidneys of patients with ANCA-associated crescentic GN and colocalize with CXCR3(+) effector T cells. To investigate the functional role of CXCR3(+) Tregs, we generated mice that lack CXCR3 in Tregs specifically (Foxp3(eGFP-Cre) × Cxcr3(fl/fl)) and induced experimental crescentic GN. Treg-specific deletion of CXCR3 resulted in reduced Treg recruitment to the kidney and an overwhelming TH1 immune response, with an aggravated course of the nephritis that was reversible on anti-IFNγ treatment. Together, these findings show that a subset of Tregs expresses CXCR3 and thereby, acquires trafficking properties of pathogenic CXCR3(+) TH1 cells, allowing Treg localization and control of excessive TH1 responses at sites of inflammation.
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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.