ArticleThe American journal of pathology2007
Protection from autoimmune diabetes and T-cell lymphoproliferation induced by FasL mutation are differentially regulated and can be uncoupled pharmacologically.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- (TCRαβCells · 2025Review
- Proximity extension assay inflammatory profiling cannot distinguish the presence of residual C-peptide in patients with long-standing type 1 diabetes.Acta diabetologica · 2025Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Beta Cell Therapies for Preventing Type 1 Diabetes: From Bench to Bedside.Biomolecules · 2020Review
- T cells genetically engineered to overcome death signaling enhance adoptive cancer immunotherapy.The Journal of clinical investigation · 2019Article
- Soluble FAS ligand is not required for pancreatic islet inflammation or beta-cell destruction in non-obese diabetic mice.Cell death discovery · 2019Article
- Expansion of FasL-Expressing CD5Frontiers in immunology · 2017Article
- 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
- B cell-targeted immunotherapy for type 1 diabetes: What can make it work?Discovery medicine · 2016Review
- From non-obese diabetic to Network for the Pancreatic Organ Donor with Diabetes: New heights in type 1 diabetes research.World journal of diabetes · 2015Article
- Double negative (DN) αβ T cells: misperception and overdue recognition.Immunology and cell biology · 2015Review
- Status of autoimmune diabetes 20-year after generation of BDC2.5-TCR transgenic non-obese diabetic mouse.World journal of diabetes · 2013Article
- The potential of Fas ligand (apoptosis-inducing molecule) as an unconventional therapeutic target in type 1 diabetes.Frontiers in immunology · 2012Article
- Inhibition of Fas ligand in NOD mice unmasks a protective role for IL-10 against insulitis development.The American journal of pathology · 2011Article
- Blocking Fas ligand on leukocytes attenuates kidney ischemia-reperfusion injury.Journal of the American Society of Nephrology : JASN · 2011Article
- Analysis of gene profile, steady state proliferation and apoptosis of double-negative T cells in the periphery and gut epithelium provides new insights into the biological functions of the Fas pathway.Immunologic research · 2010Review
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Spontaneous mutation of Fas (lpr) or FasL (gld) completely protects nonobese diabetic mice from autoimmune diabetes but also causes massive double-negative T-cell lymphoproliferation. In this study, we used bone marrow chimeras and adoptive transfer analysis to investigate further the role of FasL in the pathogenesis of autoimmune diabetes and to determine whether gld-induced tolerance and double-negative T-cell lymphoproliferation can be uncoupled from each other. We show that FasL expressed on hematopoietic and nonhematopoietic compartments plays nonredundant roles in the pathogenesis of autoimmune diabetes. Mutation of FasL in either compartment interferes with the autoimmune process and prevents onset of diabetes, but FasL expressed in the hematopoietic compartment is the dominant regulator of T-cell homeostasis. Furthermore, pathogenesis of diabetes is dependent on normal FasL expression in both compartments, whereas only minimal FasL function is required to maintain T-cell homeostasis. Consequently, partial disruption of FasL protects from autoimmune diabetes without causing T-cell lymphoproliferation. This is demonstrated genetically in nonobese diabetic-gld/+ mice and pharmacologically by using FasL-neutralizing antibody. These results have important implications for understanding the role of the Fas pathway in pathogenesis of autoimmune diseases and for designing novel FasL-modulating therapies.
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