ArticleThe American journal of pathology2011
Inhibition of Fas ligand in NOD mice unmasks a protective role for IL-10 against insulitis development.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Proximity extension assay inflammatory profiling cannot distinguish the presence of residual C-peptide in patients with long-standing type 1 diabetes.Acta diabetologica · 2025Article
- Article
- Shift in the B cell subsets between children with type 1 diabetes and/or celiac disease.Clinical and experimental immunology · 2024Article
- Understanding the Effects of Age and T-Cell Differentiation on COVID-19 Severity: Implicating a Fas/FasL-mediated Feed-Forward Controller of T-Cell Differentiation.Frontiers in immunology · 2022Article
- Regulatory B Cells in Type 1 Diabetes.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Immunosuppressive Mechanisms of Regulatory B Cells.Frontiers in immunology · 2021Review
- Dendritic cells license regulatory B cells to produce IL-10 and mediate suppression of antigen-specific CD8 T cells.Cellular & molecular immunology · 2020Article
- Current understandings of the pathogenesis of type 1 diabetes: Genetics to environment.World journal of diabetes · 2020Review
- Hybrid lipids, peptides, and lymphocytes: new era in type 1 diabetes research.The Journal of clinical investigation · 2019Article
- Article
- IL-17 and limits of success.Cellular immunology · 2019Review
- Soluble FAS ligand is not required for pancreatic islet inflammation or beta-cell destruction in non-obese diabetic mice.Cell death discovery · 2019Article
- Hiding in plain sight: time to unlock autoimmune clues in human CD5+ B cells by using nextgen technology.Discovery medicine · 2018Article
- Therapies to Suppress β Cell Autoimmunity in Type 1 Diabetes.Frontiers in immunology · 2018Review
- Circulating B cells in type 1 diabetics exhibit fewer maturation-associated phenotypes.Clinical immunology (Orlando, Fla.) · 2017Article
- Expansion of FasL-Expressing CD5Frontiers in immunology · 2017Article
- Beta-cell Specific Autoantibodies: Are they Just an Indicator of Type 1 Diabetes?Current diabetes reviews · 2017Review
- 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
- Editorial: Ying and Yang Members of the Tumor Necrosis Factor Superfamily: Friends or Foes in Immune-Mediated Diseases and Cancer.Frontiers in immunology · 2017Article
- Protective role of adenovirus vector-mediated interleukin-10 gene therapy on endogenous islet β-cells in recent-onset type 1 diabetes in NOD mice.Experimental and therapeutic medicine · 2016Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Type 1 diabetes mellitus (T1D) is an autoimmune disease caused by the destruction of pancreatic insulin-producing β cells by autoreactive T cells early in life. Despite daily insulin injections, patients typically develop cardiovascular and other complications; and intensive efforts are being directed toward identifying therapeutic targets to prevent the disease without directly impinging on the host defense. Fas ligand (FasL) is one potential target. Fas-FasL interactions primarily regulate T-cell homeostasis, not activation. Nevertheless, spontaneous gene mutation of Fas (called lpr mutation) or FasL (called the gld mutation) prevents autoimmune diabetes in nonobese diabetic (NOD) mice, the widely used model for T1D. Furthermore, although homozygous gld mutations cause age-dependent lymphoproliferation, limiting the gld mutation to one allele (NOD-gld/+) or treating NOD-wild-type mice with FasL-neutralizing monoclonal antibody completely prevents the disease development without causing lymphoproliferation or immune suppression. Herein, we show that the heterozygous gld mutation inhibits the accumulation of diabetogenic T cells in the pancreas, without interfering with their proliferation and expansion in the draining pancreatic lymph nodes. Pancreata from NOD-gld/+ mice contained B cells that expressed CD5 and produced IL-10, which was critical for maintenance of the disease resistance because its neutralization with an IL-10 receptor-blocking monoclonal antibody allowed accumulation of CD4 T cells in the pancreas and led to insulitis development. The results provide novel insights into the pathogenesis of T1D that could have important therapeutic implications.
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