ArticleDiabetologia2012
Acceleration of diabetes development in CXC chemokine receptor 3 (CXCR3)-deficient NOD mice.
Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Regulatory T cell dysfunction and immunotherapeutic breakthroughs in type 1 diabetes.Frontiers in endocrinology · 2025Review
- Genome-wide aggregated trans-effects on risk of type 1 diabetes: A test of the "omnigenic" sparse effector hypothesis of complex trait genetics.American journal of human genetics · 2023Article
- Pro-inflammatory β cell small extracellular vesicles induce β cell failure through activation of the CXCL10/CXCR3 axis in diabetes.Cell reports · 2021Article
- 12-Lipoxygenase governs the innate immune pathogenesis of islet inflammation and autoimmune diabetes.JCI insight · 2021Article
- ICOSFrontiers in immunology · 2020Review
- Estrogen regulates sex-specific localization of regulatory T cells in adipose tissue of obese female mice.PloS one · 2020Article
- Immune cell trafficking to the islets during type 1 diabetes.Clinical and experimental immunology · 2019Review
- CD11cFrontiers in immunology · 2019Article
- The islet-resident macrophage is in an inflammatory state and senses microbial products in blood.The Journal of experimental medicine · 2017Article
- Pancreatic islet inflammation: an emerging role for chemokines.Journal of molecular endocrinology · 2017Review
- Unique Features of Pancreatic-Resident Regulatory T Cells in Autoimmune Type 1 Diabetes.Frontiers in immunology · 2017Review
- Singular role for T-BET+CXCR3+ regulatory T cells in protection from autoimmune diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Article
- Urine CXCL10/IP-10 Fingers Ongoing Antibody-Mediated Kidney Graft Rejection.Journal of the American Society of Nephrology : JASN · 2015Article
- Th1-Like ICOS+ Foxp3+ Treg Cells Preferentially Express CXCR3 and Home to β-Islets during Pre-Diabetes in BDC2.5 NOD Mice.PloS one · 2015Article
- Naturally occurring anthraquinones: chemistry and therapeutic potential in autoimmune diabetes.Evidence-based complementary and alternative medicine : eCAM · 2015Review
- Macrophages and β-cells are responsible for CXCR2-mediated neutrophil infiltration of the pancreas during autoimmune diabetes.EMBO molecular medicine · 2014Article
- Article
- Altered immune regulation in type 1 diabetes.Clinical & developmental immunology · 2013Review
- The fine balance of chemokines during disease: trafficking, inflammation, and homeostasis.Methods in molecular biology (Clifton, N.J.) · 2013Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe aim of this study was to understand the role of CXC chemokine receptor 3 (CXCR3), a T-helper 1(Th1) type chemokine receptor, in the pathogenesis of type 1 diabetes.
methodsWe observed the incidence of diabetes in Cxcr3 homozygous knockout mice. We compared the expression pattern of various cytokines and chemokines and the frequency of FOXP3(+) cells in the pancreas and pancreatic lymph nodes from Cxcr3 ( -/- ) NOD mice and wild-type NOD mice. In addition, we observed the migration ability of CXCR3(+)CD4(+) cells to pancreatic islets upon adoptive transfer. Finally, we examined whether Cxcr3 (+) regulatory T cells (Tregs) actually suppressed the onset of diabetes in vivo.
resultsCxcr3 ( -/- ) NOD mice developed spontaneous diabetes earlier than did wild-type NOD mice. In Cxcr3 ( -/- ) NOD mice, Tregs were more frequent in pancreatic lymph nodes and less frequent in pancreatic islets than in wild-type NOD mice. While transferred CXCR3(-)CD4(+) cells from wild-type NOD mice did not infiltrate pancreatic islets of NOD-severe combined immunodeficiency (SCID) mice, CXCR3(+)CD4(+) cells from the same mice migrated into the recipient islets and contained Forkhead box P3 (FOXP3) upon adoptive transfer. Moreover, CD4(+)CD25(+) cells from wild-type NOD mice suppressed and delayed the onset of diabetes compared with those from Cxcr3 ( -/- ) NOD mice in a cyclophosphamide-induced diabetes model system. CONCLUSIONS/
interpretationThe mechanism of accelerated diabetes onset in Cxcr3 ( -/- ) NOD mice was considered to be due to the lack of hybrid Tregs (CXCR3(+)FOXP3(+)CD4(+) cells), which could effectively migrate into and regulate Th1 inflammation in local lesions under Cxcr3 knockout conditions.
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