Beta cell MHC class I is a late requirement for diabetes - Wikidata - awgldk - TriplyDB

Beta cell MHC class I is a late requirement for diabetes

Beta cell MHC class I is a late requirement for diabetes

http://www.wikidata.org/entity/Q35143964

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Positive evidence for vitamin A role in prevention of type 1 diabetes Pancreas-specific Cre driver lines and considerations for their prudent use miRNAs: novel regulators of autoimmunity-mediated pancreatic β-cell destruction in type 1 diabetes.In situ recognition of autoantigen as an essential gatekeeper in autoimmune CD8+ T cell inflammation Islet-specific CTL cloned from a type 1 diabetes patient cause beta-cell destruction after engraftment into HLA-A2 transgenic NOD/scid/IL2RG null mice.Ins1(Cre) knock-in mice for beta cell-specific gene recombination.Autoreactive cytotoxic T lymphocytes acquire higher expression of cytotoxic effector markers in the islets of NOD mice after priming in pancreatic lymph nodes TRAIL modulates the immune system and protects against the development of diabetes.Beta cells cannot directly prime diabetogenic CD8 T cells in nonobese diabetic mice.Resistance of the target islet tissue to autoimmune destruction contributes to genetic susceptibility in Type 1 diabetes.Heterogeneity and Lobularity of Pancreatic Pathology in Type 1 Diabetes during the Prediabetic Phase The good turned ugly: immunopathogenic basis for diabetogenic CD8+ T cells in NOD mice.B-cell cross-presentation of autologous antigen precipitates diabetes.The vicious cycle of apoptotic beta-cell death in type 1 diabetes.Genetically engineered human islets protected from CD8-mediated autoimmune destruction in vivo.Pathogenic mechanisms in type 1 diabetes: the islet is both target and driver of disease.Altered immune regulation in type 1 diabetes.T cell islet accumulation in type 1 diabetes is a tightly regulated, cell-autonomous event The role of perforin and granzymes in diabetes.Viruses and cytotoxic T lymphocytes in type 1 diabetes.Type 1 diabetes: etiology, immunology, and therapeutic strategies.Antigen presentation events in autoimmune diabetes.The role of reactive oxygen species and proinflammatory cytokines in type 1 diabetes pathogenesis.Advances in our understanding of the pathophysiology of Type 1 diabetes: lessons from the NOD mouse.Mechanisms of diabetic autoimmunity: I--the inductive interface between islets and the immune system at onset of inflammation.Mechanisms of autoimmunity in the non-obese diabetic mouse: effector/regulatory cell equilibrium during peak inflammation.An indirect role for NK cells in a CD4(+) T-cell-dependent mouse model of type I diabetes.Perforin facilitates beta cell killing and regulates autoreactive CD8+ T-cell responses to antigen in mouse models of type 1 diabetes.Internalization and presentation of myelin antigens by the brain endothelium guides antigen-specific T cell migration.Intracellular pathways of pancreatic β-cell apoptosis in type 1 diabetes.The CD19 signalling molecule is elevated in NOD mice and controls type 1 diabetes development.In vivo effects of cytokines on pancreatic beta-cells in models of type I diabetes dependent on CD4(+) T lymphocytes.Induction of CD4+CD25+Foxp3+ regulatory T cell response by glatiramer acetate in type 1 diabetes.T Cell-Mediated Beta Cell Destruction: Autoimmunity and Alloimmunity in the Context of Type 1 Diabetes.Mouse pancreatic beta cells express MHC class II and stimulate CD4(+) T cells to proliferate.Autoreactive T cells induce necrosis and not BCL-2-regulated or death receptor-mediated apoptosis or RIPK3-dependent necroptosis of transplanted islets in a mouse model of type 1 diabetes.In Vivo Analysis of miR-34a Regulated Glucose Metabolism Related Genes in

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Beta cell MHC class I is a late requirement for diabetes

http://www.wikidata.org/entity/Q35143964

description

2003 nî lūn-bûn

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2003 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2003 թվականի մայիսին հրատարակված գիտական հոդված

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2003年の論文

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2003年論文

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2003年論文

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2003年論文

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2003年論文

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2003年論文

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2003年论文

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name

Beta cell MHC class I is a late requirement for diabetes

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Beta cell MHC class I is a late requirement for diabetes

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type

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Beta cell MHC class I is a late requirement for diabetes

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Beta cell MHC class I is a late requirement for diabetes

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prefLabel

Beta cell MHC class I is a late requirement for diabetes

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Beta cell MHC class I is a late requirement for diabetes

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PNAS.1131954100

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Proceedings of the National Academy of Sciences of the United States of America

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Beta cell MHC class I is a late requirement for diabetes

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P2093

Brett Charlton

http://www.w3.org/2001/XMLSchema#string

Robyn M Slattery

http://www.w3.org/2001/XMLSchema#string

Stephanie E Palmer

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Perforin-independent beta-cell destruction by diabetogenic CD8(+) T lymphocytes in transgenic nonobese diabetic mice

Dendritic cells are sufficient to cross-present self-antigens to CD8 T cells in vivo.

IL-1alpha, IL-1beta, and IFN-gamma mark beta cells for Fas-dependent destruction by diabetogenic CD4(+) T lymphocytes

Transgenic rescue implicates beta2-microglobulin as a diabetes susceptibility gene in nonobese diabetic (NOD) mice

Identification of a new susceptibility locus for insulin-dependent diabetes mellitus by ancestral haplotype congenic mapping

Determinants of the selective toxicity of alloxan to the pancreatic B cell.

MHC antigen induction by interferon gamma on cultured mouse pancreatic beta cells and macrophages. Genetic analysis of strain differences and discovery of an "occult" class I-like antigen in NOD/Lt mice

Pancreatic islet beta cells drive T cell-immune responses in the nonobese diabetic mouse model.

Reduced incidence and delayed onset of diabetes in perforin-deficient nonobese diabetic mice.

Major histocompatibility complex class I-restricted cross-presentation is biased towards high dose antigens and those released during cellular destruction

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6688-6693

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scholarly article

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10.1073/PNAS.1131954100

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11

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100

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Emma E Hamilton-Williams

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2003-05-15T00:00:00Z

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10757608

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12750472

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164508

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