ArticleEuropean journal of immunology2011
In vivo diabetogenic action of CD4+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18.
Article in European journal of immunology, 2011. 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, 14 citations in OpenAlex.
- The trigger for pancreatic disease: NLRP3 inflammasome.Cell death discovery · 2023Review
- The regulation of self-tolerance and the role of inflammasome molecules.Frontiers in immunology · 2023Review
- Inflammasomes and Type 1 Diabetes.Frontiers in immunology · 2021Review
- 100 years post-insulin: immunotherapy as the next frontier in type 1 diabetes.Immunotherapy advances · 2021Review
- The NLRP3 Inflammasome and Its Role in T1DM.Frontiers in immunology · 2020Review
- Fas/Fas-Ligand Interaction As a Mechanism of Immune Homeostasis and β-Cell Cytotoxicity: Enforcement Rather Than Neutralization for Treatment of Type 1 Diabetes.Frontiers in immunology · 2017Article
- The role of the innate immune system in destruction of pancreatic beta cells in NOD mice and humans with type I diabetes.Journal of autoimmunity · 2016Review
- NLRP3 deficiency protects from type 1 diabetes through the regulation of chemotaxis into the pancreatic islets.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Therapy: Immunotherapy for T1DM--targeting innate immunity.Nature reviews. Endocrinology · 2013Article
- Type 1 diabetes therapy beyond T cell targeting: monocytes, B cells, and innate lymphocytes.The review of diabetic studies : RDS · 2012Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
CD4(+) T lymphocytes are required to induce spontaneous autoimmune diabetes in the NOD mouse. Since pancreatic β cells upregulate Fas expression upon exposure to pro-inflammatory cytokines, we studied whether the diabetogenic action of CD4(+) T lymphocytes depends on Fas expression on target cells. We assayed the diabetogenic capacity of NOD spleen CD4(+) T lymphocytes when adoptively transferred into a NOD mouse model combining: (i) Fas-deficiency, (ii) FasL-deficiency, and (iii) SCID mutation. We found that CD4(+) T lymphocytes require Fas expression in the recipients' target cells to induce diabetes. IL-1β has been described as a key cytokine involved in Fas upregulation on mouse β cells. We addressed whether CD4(+) T cells require IL-1β to induce diabetes. We also studied spontaneous diabetes onset in NOD/IL-1 converting enzyme-deficient mice, in NOD/IL-1β-deficient mice, and CD4(+) T-cell adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. Neither IL-1β nor IL-18 are required for either spontaneous or CD4(+) T-cell adoptively transferred diabetes. We conclude that CD4(+) T-cell-mediated β-cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo.
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