B lymphocyte "original sin" in the bone marrow enhances islet autoreactivity in type 1 diabetes-prone nonobese diabetic mice - Wikidata - wikimedia - TriplyDB

B lymphocyte "original sin" in the bone marrow enhances islet autoreactivity in type 1 diabetes-prone nonobese diabetic mice

B lymphocyte "original sin" in the bone marrow enhances islet autoreactivity in type 1 diabetes-prone nonobese diabetic mice

http://www.wikidata.org/entity/Q36920508

about

NFATc2 (NFAT1) assists BCR-mediated anergy in anti-insulin B cells Loss of anergic B cells in prediabetic and new-onset type 1 diabetic patients.The importance of the Non Obese Diabetic (NOD) mouse model in autoimmune diabetes Reversing Tolerance in Isotype Switch-Competent Anti-Insulin B Lymphocytes.Bruton's Tyrosine Kinase Synergizes with Notch2 To Govern Marginal Zone B Cells in Nonobese Diabetic Mice.Targeting Anti-Insulin B Cell Receptors Improves Receptor Editing in Type 1 Diabetes-Prone Mice.Class-switched anti-insulin antibodies originate from unconventional antigen presentation in multiple lymphoid sites.B Cell Receptor Affinity for Insulin Dictates Autoantigen Acquisition and B Cell Functionality in Autoimmune Diabetes.The human dark side: evolutionary psychology and original sin.Genetic and Small Molecule Disruption of the AID/RAD51 Axis Similarly Protects Nonobese Diabetic Mice from Type 1 Diabetes through Expansion of Regulatory B Lymphocytes.Mechanisms of central tolerance for B cells.Genetic, Cellular and Clinical Features of ICF Syndrome: a French National Survey.

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B lymphocyte "original sin" in the bone marrow enhances islet autoreactivity in type 1 diabetes-prone nonobese diabetic mice

http://www.wikidata.org/entity/Q36920508

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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name

B lymphocyte "original sin" in ...... s-prone nonobese diabetic mice

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JIMMUNOL.1201359

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Journal of Immunology

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B lymphocyte "original sin" in ...... s-prone nonobese diabetic mice

@en

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Amita B Rachakonda

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

James W Thomas

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

Jonathan M Williams

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

Mariam Karamali

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Peggy L Kendall

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Rachel A Henry-Bonami

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P2860

Receptor editing is the main mechanism of B cell tolerance toward membrane antigens

Predominant autoantibody production by early human B cell precursors

Cannabinoid receptor 2 mediates the retention of immature B cells in bone marrow sinusoids

Anergy and not clonal ignorance determines the fate of B cells that recognize a physiological autoantigen.

S1P3 confers differential S1P-induced migration by autoreactive and non-autoreactive immature B cells and is required for normal B-cell development.

In vivo activity and in vitro specificity of CD4+ Th1 and Th2 cells derived from the spleens of diabetic NOD mice.

Vkappa polymorphisms in NOD mice are spread throughout the entire immunoglobulin kappa locus and are shared by other autoimmune strains

Reduced diabetes in btk-deficient nonobese diabetic mice and restoration of diabetes with provision of an anti-insulin IgH chain transgene

Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice.

Age of islet autoantibody appearance and mean levels of insulin, but not GAD or IA-2 autoantibodies, predict age of diagnosis of type 1 diabetes: diabetes autoimmunity study in the young.

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5992-6003

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10.4049/JIMMUNOL.1201359

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12

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190

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2013-05-15T00:00:00Z

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236912160

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23677466

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type-1 diabetes

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3679359

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