Analysis of the spontaneous T cell response to insulin in NOD mice.
about
Insulin expressing hepatocytes not destroyed in transgenic NOD miceProtection of nonobese diabetic mice from diabetes by intranasal or subcutaneous administration of insulin peptide B-(9-23)Prevention of type I diabetes transfer by glutamic acid decarboxylase 65 peptide 206-220-specific T cellsBDC12-4.1 T-cell receptor transgenic insulin-specific CD4 T cells are resistant to in vitro differentiation into functional Foxp3+ T regulatory cells.TGF-beta signaling is required for the function of insulin-reactive T regulatory cellsThymus-specific deletion of insulin induces autoimmune diabetes.Unique autoreactive T cells recognize insulin peptides generated within the islets of Langerhans in autoimmune diabetes.A pancreatic beta-cell-specific homolog of glucose-6-phosphatase emerges as a major target of cell-mediated autoimmunity in diabetesRegister shifting of an insulin peptide-MHC complex allows diabetogenic T cells to escape thymic deletionAntigen-specific therapeutic approaches in Type 1 diabetesT cell receptor restriction of diabetogenic autoimmune NOD T cellsThe stages of type 1A diabetes: 2005.Interferon-gamma is essential for destruction of beta cells and development of insulin-dependent diabetes mellitus.Antigen-specific therapy for autoimmune disease: prospects for the prevention of insulin-dependent diabetesIntranasal administration of insulin peptide B: 9-23 protects NOD mice from diabetes.Antigen presentation events during the initiation of autoimmune diabetes in the NOD mouseThe role of islet antigen presenting cells and the presentation of insulin in the initiation of autoimmune diabetes in the NOD mouse.Pathogenic CD4⁺ T cells recognizing an unstable peptide of insulin are directly recruited into islets bypassing local lymph nodes.Oral insulin treatment suppresses virus-induced antigen-specific destruction of beta cells and prevents autoimmune diabetes in transgenic mice.Metabolically inactive insulin analog prevents type I diabetes in prediabetic NOD miceT cell islet accumulation in type 1 diabetes is a tightly regulated, cell-autonomous eventNo effect of the altered peptide ligand NBI-6024 on beta-cell residual function and insulin needs in new-onset type 1 diabetes.Proinsulin Expression Shapes the TCR Repertoire but Fails to Control the Development of Low-Avidity Insulin-Reactive CD8+ T Cells.Antigen-specific therapy against type 1 diabetes: mechanisms and perspectives.The CD19 signalling molecule is elevated in NOD mice and controls type 1 diabetes development.C-terminal modification of the insulin B:11-23 peptide creates superagonists in mouse and human type 1 diabetes.
P2860
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P2860
Analysis of the spontaneous T cell response to insulin in NOD mice.
description
1994 nî lūn-bûn
@nan
1994年の論文
@ja
1994年論文
@yue
1994年論文
@zh-hant
1994年論文
@zh-hk
1994年論文
@zh-mo
1994年論文
@zh-tw
1994年论文
@wuu
1994年论文
@zh
1994年论文
@zh-cn
name
Analysis of the spontaneous T cell response to insulin in NOD mice.
@ast
Analysis of the spontaneous T cell response to insulin in NOD mice.
@en
type
label
Analysis of the spontaneous T cell response to insulin in NOD mice.
@ast
Analysis of the spontaneous T cell response to insulin in NOD mice.
@en
prefLabel
Analysis of the spontaneous T cell response to insulin in NOD mice.
@ast
Analysis of the spontaneous T cell response to insulin in NOD mice.
@en
P2093
P356
P1476
Analysis of the spontaneous T cell response to insulin in NOD mice.
@en
P2093
Norbury-Glaser M
Wegmann DR
P304
P356
10.1006/JAUT.1994.1066
P577
1994-12-01T00:00:00Z