CD8( ) T cells specific for beta cells encounter their cognate antigens in the islets of NOD mice. (Q44132086)

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4 February 2020

title

CD8( ) T cells specific for beta cells encounter their cognate antigens in the islets of NOD mice (English)

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9

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8

Roland Tisch

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10

Bo Wang

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author name string

Shuguang Pang

1

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Li Zhang

2

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Haidong Wang

3

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4 February 2020

Zuoan Yi

4

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Li Li

5

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Ling Gao

6

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Jiajun Zhao

7

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language of work or name

English

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publication date

1 October 2009

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European Journal of Immunology

4 February 2020

published in

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volume

39

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issue

10

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page(s)

2716-2724

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Helper requirements for generation of effector CTL to islet beta cell antigens

4 February 2020

cites work

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Individual nonobese diabetic mice exhibit unique patterns of CD8 T cell reactivity to three islet antigens, including the newly identified widely expressed dystrophia myotonica kinase

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CD8 T cell tolerance in nonobese diabetic mice is restored by insulin-dependent diabetes resistance alleles.

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In situ beta cell death promotes priming of diabetogenic CD8 T lymphocytes

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Cross-priming of diabetogenic T cells dissociated from CTL-induced shedding of beta cell autoantigens.

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Adoptive transfer of diabetes into immunodeficient NOD-scid/scid mice. Relative contributions of CD4 and CD8 T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors

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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

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Transplanted MHC class I-deficient nonobese diabetic mouse islets are protected from autoimmune injury in diabetic nonobese recipients

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Beta cell MHC class I is a late requirement for diabetes

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Beta cells cannot directly prime diabetogenic CD8 T cells in nonobese diabetic mice

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The role of lymphocyte subsets in accelerated diabetes in nonobese diabetic-rat insulin promoter-B7-1 (NOD-RIP-B7-1) mice

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Identification of a CD8 T cell that can independently mediate autoimmune diabetes development in the complete absence of CD4 T cell helper functions

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Exclusive Expression of MHC Class II Proteins on CD45 Cells in Pancreatic Islets of NOD Mice

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The Use of Idd Congenic Mice to Identify Checkpoints of Peripheral Tolerance to Islet Antigen

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The molecular program induced in T cells undergoing homeostatic proliferation

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Initiation of autoimmune diabetes by developmentally regulated presentation of islet cell antigens in the pancreatic lymph nodes

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Major histocompatibility complex class I molecules are required for the development of insulitis in non-obese diabetic mice

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Major histocompatibility complex class I-deficient NOD-B2mnull mice are diabetes and insulitis resistant

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Prevention of insulitis and diabetes in beta 2-microglobulin-deficient non-obese diabetic mice

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Beta 2-microglobulin-deficient NOD mice do not develop insulitis or diabetes

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The role of CD8 T cells in the initiation of insulin-dependent diabetes mellitus

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Physiological β Cell Death Triggers Priming of Self-reactive T Cells by Dendritic Cells in a Type-1 Diabetes Model

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CD4 T cells are sufficient to elicit allograft rejection and major histocompatibility complex class I molecule is required to induce recurrent autoimmune diabetes after pancreas transplantation in mice

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7 January 2021

Indefinite survival of MHC class I-deficient murine pancreatic islet allografts

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CD28-mediated signalling co-stimulates murine T cells and prevents induction of anergy in T-cell clones

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7 January 2021

Neonatal tumor necrosis factor alpha promotes diabetes in nonobese diabetic mice by CD154-independent antigen presentation to CD8( ) T cells.

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Costimulator B7-1 confers antigen-presenting-cell function to parenchymal tissue and in conjunction with tumor necrosis factor alpha leads to autoimmunity in transgenic mice

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Independent control of immunoglobulin switch recombination at individual switch regions evidenced through Cre-loxP-mediated gene targeting

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Defective CD8 T Cell Peripheral Tolerance in Nonobese Diabetic Mice

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