Major histocompatibility complex class I-restricted T cells are required for all but the end stages of diabetes development in nonobese diabetic mice and use a prevalent T cell receptor alpha chain gene rearrangement
about
Identification of the beta cell antigen targeted by a prevalent population of pathogenic CD8+ T cells in autoimmune diabetes.Predominant occupation of the class I MHC molecule H-2Kwm7 with a single self-peptide suggests a mechanism for its diabetes-protective effect.Functional evidence for the mediation of diabetogenic T cell responses by HLA-A2.1 MHC class I molecules through transgenic expression in NOD mice.Rapid identification of MHC class I-restricted antigens relevant to autoimmune diabetes using retrogenic T cells.Idd9.1 locus controls the suppressive activity of FoxP3+CD4+CD25+ regulatory T-cellsTumor necrosis factor-alpha and the progression of diabetes in non-obese diabetic mice.Role of autoreactive CD8+ T cells in organ-specific autoimmune diseases: insight from transgenic mouse models.Ins2 deficiency augments spontaneous HLA-A*0201-restricted T cell responses to insulin.Developmental control of CD8 T cell-avidity maturation in autoimmune diabetes.Perforin-independent beta-cell destruction by diabetogenic CD8(+) T lymphocytes in transgenic nonobese diabetic miceInterleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity.The pathogenicity of self-antigen decreases at high levels of autoantigenicity: a computational approach.Compensatory mechanisms allow undersized anchor-deficient class I MHC ligands to mediate pathogenic autoreactive T cell responsesT cells recognizing a peptide contaminant undetectable by mass spectrometry.Autoreactive CD8 T cells associated with beta cell destruction in type 1 diabetesRAG-dependent peripheral T cell receptor diversification in CD8+ T lymphocytesAutoreactive effector/memory CD4+ and CD8+ T cells infiltrating grafted and endogenous islets in diabetic NOD mice exhibit similar T cell receptor usage.Prevention of "Humanized" diabetogenic CD8 T-cell responses in HLA-transgenic NOD mice by a multipeptide coupled-cell approachOxidative stress and redox modulation potential in type 1 diabetes.A pancreatic beta-cell-specific homolog of glucose-6-phosphatase emerges as a major target of cell-mediated autoimmunity in diabetesProteasome immunosubunits protect against the development of CD8 T cell-mediated autoimmune diseasesResponses against islet antigens in NOD mice are prevented by tolerance to proinsulin but not IGRP.Prevalent CD8(+) T cell response against one peptide/MHC complex in autoimmune diabetes.Development of new strategies to prevent type 1 diabetes: the role of animal models.The importance of the Non Obese Diabetic (NOD) mouse model in autoimmune diabetesMaking the most of major histocompatibility complex molecule multimers: applications in type 1 diabetes.The Presence and Preferential Activation of Regulatory T Cells Diminish Adoptive Transfer of Autoimmune Diabetes by Polyclonal Nonobese Diabetic (NOD) T Cell Effectors into NSG versus NOD-scid MiceThe good turned ugly: immunopathogenic basis for diabetogenic CD8+ T cells in NOD mice.Islet autoantigens: structure, function, localization, and regulation.The use of peptide-major-histocompatibility-complex multimers in type 1 diabetes mellitus.B7x in the periphery abrogates pancreas-specific damage mediated by self-reactive CD8 T cells.T-bet controls autoaggressive CD8 lymphocyte responses in type 1 diabetes.Functional characterization of T cell populations in a mouse model of chronic obstructive pulmonary diseaseRotavirus infection accelerates type 1 diabetes in mice with established insulitisIdd9/11 genetic locus regulates diabetogenic activity of CD4 T-cells in nonobese diabetic (NOD) mice.CD40 interacts directly with RAG1 and RAG2 in autoaggressive T cells and Fas prevents CD40-induced RAG expression.Breaking T cell tolerance to beta cell antigens by merocytic dendritic cellsT cell islet accumulation in type 1 diabetes is a tightly regulated, cell-autonomous eventCD8+ T cells specific for the islet autoantigen IGRP are restricted in their T cell receptor chain usage.The role of reactive oxygen species and proinflammatory cytokines in type 1 diabetes pathogenesis.
P2860
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P2860
Major histocompatibility complex class I-restricted T cells are required for all but the end stages of diabetes development in nonobese diabetic mice and use a prevalent T cell receptor alpha chain gene rearrangement
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
Major histocompatibility compl ...... alpha chain gene rearrangement
@ast
Major histocompatibility compl ...... alpha chain gene rearrangement
@en
type
label
Major histocompatibility compl ...... alpha chain gene rearrangement
@ast
Major histocompatibility compl ...... alpha chain gene rearrangement
@en
prefLabel
Major histocompatibility compl ...... alpha chain gene rearrangement
@ast
Major histocompatibility compl ...... alpha chain gene rearrangement
@en
P2093
P2860
P356
P1476
Major histocompatibility compl ...... alpha chain gene rearrangement
@en
P2093
D C Roopenian
D V Serreze
G J Christianson
H D Chapman
R T Graser
S G Nathenson
T P DiLorenzo
P2860
P304
12538-12543
P356
10.1073/PNAS.95.21.12538
P407
P577
1998-10-01T00:00:00Z