Perforin-independent beta-cell destruction by diabetogenic CD8(+) T lymphocytes in transgenic nonobese diabetic mice
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Innate immunity and intestinal microbiota in the development of Type 1 diabetesIL-1alpha, IL-1beta, and IFN-gamma mark beta cells for Fas-dependent destruction by diabetogenic CD4(+) T lymphocytesGranzyme B is dispensable in the development of diabetes in non-obese diabetic mice.Contribution of Fas to diabetes development.Perforin: structure, function, and role in human immunopathology.Intracellular versus extracellular granzyme B in immunity and disease: challenging the dogma.Oxidative stress and redox modulation potential in type 1 diabetes.Beta cell MHC class I is a late requirement for diabetesApoptosis in autoimmune diabetes: the fate of beta-cells in the cleft between life and death.Apoptosis of human islet cells by cytokines.Cytotoxic mechanisms employed by mouse T cells to destroy pancreatic β-cells.B-cell cross-presentation of autologous antigen precipitates diabetes.T-bet controls autoaggressive CD8 lymphocyte responses in type 1 diabetes.The vicious cycle of apoptotic beta-cell death in type 1 diabetes.Accelerated type 1 diabetes induction in mice by adoptive transfer of diabetogenic CD4+ T cells.Pathogenic mechanisms in type 1 diabetes: the islet is both target and driver of disease.The role of perforin and granzymes in diabetes.MDA5 Is Critical to Host Defense during Infection with Murine Coronavirus.Neutralization Versus Reinforcement of Proinflammatory Cytokines to Arrest Autoimmunity in Type 1 Diabetes.Perforin facilitates beta cell killing and regulates autoreactive CD8+ T-cell responses to antigen in mouse models of type 1 diabetes.Fas/Fas-Ligand Interaction As a Mechanism of Immune Homeostasis and β-Cell Cytotoxicity: Enforcement Rather Than Neutralization for Treatment of Type 1 Diabetes.Effective destruction of Fas-deficient insulin-producing beta cells in type 1 diabetes.Intracellular pathways of pancreatic β-cell apoptosis in type 1 diabetes.The pro-apoptotic BH3-only protein Bid is dispensable for development of insulitis and diabetes in the non-obese diabetic mouse.In vivo effects of cytokines on pancreatic beta-cells in models of type I diabetes dependent on CD4(+) T lymphocytes.Mitochondrial Reactive Oxygen Species and Type 1 Diabetes.Genetic deletion of granzyme B does not confer resistance to the development of spontaneous diabetes in non-obese diabetic mice.The Type 1 Diabetes PhysioLab Platform: a validated physiologically based mathematical model of pathogenesis in the non-obese diabetic mouse.Heterozygosity for the common perforin mutation, p.A91V, impairs the cytotoxicity of primary natural killer cells from healthy individualsPerforin and Fas induced by IFNγ and TNFα mediate beta cell death by OT-I CTL
P2860
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P2860
Perforin-independent beta-cell destruction by diabetogenic CD8(+) T lymphocytes in transgenic nonobese diabetic mice
description
1999 nî lūn-bûn
@nan
1999 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Perforin-independent beta-cell ...... nsgenic nonobese diabetic mice
@ast
Perforin-independent beta-cell ...... nsgenic nonobese diabetic mice
@en
type
label
Perforin-independent beta-cell ...... nsgenic nonobese diabetic mice
@ast
Perforin-independent beta-cell ...... nsgenic nonobese diabetic mice
@en
prefLabel
Perforin-independent beta-cell ...... nsgenic nonobese diabetic mice
@ast
Perforin-independent beta-cell ...... nsgenic nonobese diabetic mice
@en
P2093
P2860
P356
P1476
Perforin-independent beta-cell ...... nsgenic nonobese diabetic mice
@en
P2093
P2860
P304
P356
10.1172/JCI6266
P407
P577
1999-04-01T00:00:00Z