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Editorial: Genetic basis of tolerance induction defects underlying the development of autoimmune pathologies

Frontiers in immunology, 2022-10, Vol.13, p.1069232-1069232

2022

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HLA-B39:06 Efficiently Mediates Type 1 Diabetes in a Mouse Model Incorporating Reduced Thymic Insulin Expression

The Journal of immunology (1950), 2018-05, Vol.200 (10), p.3353-3363

2018

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Improved Murine MHC-Deficient HLA Transgenic NOD Mouse Models for Type 1 Diabetes Therapy Development

Diabetes (New York, N.Y.), 2018-05, Vol.67 (5), p.923-935

2018

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HLA-DQ8 Supports Development of Insulitis Mediated by Insulin-Reactive Human TCR-Transgenic T Cells in Nonobese Diabetic Mice

The Journal of immunology (1950), 2023-12, Vol.211 (12), p.1792

2023

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Nfkbid Overexpression in Nonobese Diabetic Mice Elicits Complete Type 1 Diabetes Resistance in Part Associated with Enhanced Thymic Deletion of Pathogenic CD8 T Cells and Increased Numbers and Activity of Regulatory T Cells

The Journal of immunology (1950), 2022-07, Vol.209 (2), p.227-237

2022

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Murine MHC-Deficient Nonobese Diabetic Mice Carrying Human HLA-DQ8 Develop Severe Myocarditis and Myositis in Response to Anti-PD-1 Immune Checkpoint Inhibitor Cancer Therapy

The Journal of immunology (1950), 2024-04, Vol.212 (8), p.1287

2024

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Transient BAFF Blockade Inhibits Type 1 Diabetes Development in Nonobese Diabetic Mice by Enriching Immunoregulatory B Lymphocytes Sensitive to Deletion by Anti-CD20 Cotherapy

The Journal of immunology (1950), 2017-12, Vol.199 (11), p.3757-3770

2017

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MHC-mismatched mixed chimerism restores peripheral tolerance of noncross-reactive autoreactive T cells in NOD mice

Proceedings of the National Academy of Sciences - PNAS, 2018-03, Vol.115 (10), p.E2329-E2337

2018

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A Hypermorphic Nfkbid Allele Contributes to Impaired Thymic Deletion of Autoreactive Diabetogenic CD8 + T Cells in NOD Mice

The Journal of immunology (1950), 2018-10, Vol.201 (7), p.1907-1917

2018

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MHC-mismatched mixed chimerism mediates thymic deletion of cross-reactive autoreactive T cells and prevents insulitis in nonobese diabetic mice

The Journal of immunology (1950), 2015-01, Vol.194 (1), p.407-417

2015

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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

The Journal of immunology (1950), 2017-06, Vol.198 (11), p.4255-4267

2017

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Interferon-γ Limits Diabetogenic CD8 + T-Cell Effector Responses in Type 1 Diabetes

Diabetes (New York, N.Y.), 2017-03, Vol.66 (3), p.710-721

2017

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T Cells from NOD- PerIg Mice Target Both Pancreatic and Neuronal Tissue

The Journal of immunology (1950), 2020-10, Vol.205 (8), p.2026-2038

2020

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Induction of Mixed Chimerism Depletes Pre-existing and De Novo-Developed Autoreactive B Cells in Autoimmune NOD Mice

Diabetes (New York, N.Y.), 2014-06, Vol.63 (6), p.2051-2062

2014

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Mixed chimerism and growth factors augment β cell regeneration and reverse late-stage type 1 diabetes

Science translational medicine, 2012-05, Vol.4 (133), p.133ra59

2012

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Antibiotic-associated Manipulation of the Gut Microbiota and Phenotypic Restoration in NOD Mice

Comparative medicine, 2017-08, Vol.67 (4), p.335-343

2017

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Administration of Anti-CD20 mAb Is Highly Effective in Preventing but Ineffective in Treating Chronic Graft-Versus-Host Disease While Preserving Strong Graft-Versus-Leukemia Effects

Biology of blood and marrow transplantation, 2014-08, Vol.20 (8), p.1089-1103

2014

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Induction of Chimerism Permits Low-Dose Islet Grafts in the Liver or Pancreas to Reverse Refractory Autoimmune Diabetes

Diabetes (New York, N.Y.), 2010-09, Vol.59 (9), p.2228-2236

2010

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A hypomorphic Ephb2 gene variant contributes to autoimmune diabetes in NOD mice associated with altered Mapk3 activities in B-lymphocytes

The Journal of immunology (1950), 2019-05, Vol.202 (1_Supplement), p.50-50.6

2019

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PLGA-microsphere delivery of insulin and IGRP epitopes as a therapy for type 1 diabetes

The Journal of immunology (1950), 2018-05, Vol.200 (1_Supplement), p.176-176.12

2018

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Nfkbid overexpression in NOD mice elicits complete type 1 diabetes resistance in part associated with enhanced thymic deletion of pathogenic CD8 T-cells and increased numbers and activity of regulatory T-cells.1,2,3

The Journal of immunology (1950), 2022-06, Vol.209 (2), p.227-237

2022

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Nfkbid overexpression in NOD mice elicits complete type 1 diabetes resistance

The Journal of immunology (1950), 2019-05, Vol.202 (1_Supplement), p.115-115.8

2019

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HLA-B39:06 Efficiently Mediates Type 1 Diabetes in a Mouse Model Incorporating Reduced Thymic Insulin Expression1

The Journal of immunology (1950), 2018-04, Vol.200 (10), p.3353-3363

2018

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Transient BAFF blockade inhibits type 1 diabetes development in NOD mice by enriching immunoregulatory B-lymphocytes sensitive to deletion by anti-CD20 co-therapy1, 2

The Journal of immunology (1950), 2017-10, Vol.199 (11), p.3757-3770

2017

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T cells from NOD-PerIg mice target both pancreatic and neuronal tissue1,2

The Journal of immunology (1950), 2020-09, Vol.205 (8), p.2026-2038

2020

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Editorial: Genetic basis of tolerance induction defects underlying the development of autoimmune pathologies

HLA-B39:06 Efficiently Mediates Type 1 Diabetes in a Mouse Model Incorporating Reduced Thymic Insulin Expression

Improved Murine MHC-Deficient HLA Transgenic NOD Mouse Models for Type 1 Diabetes Therapy Development

HLA-DQ8 Supports Development of Insulitis Mediated by Insulin-Reactive Human TCR-Transgenic T Cells in Nonobese Diabetic Mice

Nfkbid Overexpression in Nonobese Diabetic Mice Elicits Complete Type 1 Diabetes Resistance in Part Associated with Enhanced Thymic Deletion of Pathogenic CD8 T Cells and Increased Numbers and Activity of Regulatory T Cells

Murine MHC-Deficient Nonobese Diabetic Mice Carrying Human HLA-DQ8 Develop Severe Myocarditis and Myositis in Response to Anti-PD-1 Immune Checkpoint Inhibitor Cancer Therapy

Transient BAFF Blockade Inhibits Type 1 Diabetes Development in Nonobese Diabetic Mice by Enriching Immunoregulatory B Lymphocytes Sensitive to Deletion by Anti-CD20 Cotherapy

MHC-mismatched mixed chimerism restores peripheral tolerance of noncross-reactive autoreactive T cells in NOD mice

A Hypermorphic Nfkbid Allele Contributes to Impaired Thymic Deletion of Autoreactive Diabetogenic CD8 + T Cells in NOD Mice

MHC-mismatched mixed chimerism mediates thymic deletion of cross-reactive autoreactive T cells and prevents insulitis in nonobese diabetic mice

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

Interferon-γ Limits Diabetogenic CD8 + T-Cell Effector Responses in Type 1 Diabetes

T Cells from NOD- PerIg Mice Target Both Pancreatic and Neuronal Tissue

Induction of Mixed Chimerism Depletes Pre-existing and De Novo-Developed Autoreactive B Cells in Autoimmune NOD Mice

Mixed chimerism and growth factors augment β cell regeneration and reverse late-stage type 1 diabetes

Antibiotic-associated Manipulation of the Gut Microbiota and Phenotypic Restoration in NOD Mice

Administration of Anti-CD20 mAb Is Highly Effective in Preventing but Ineffective in Treating Chronic Graft-Versus-Host Disease While Preserving Strong Graft-Versus-Leukemia Effects

Induction of Chimerism Permits Low-Dose Islet Grafts in the Liver or Pancreas to Reverse Refractory Autoimmune Diabetes

A hypomorphic Ephb2 gene variant contributes to autoimmune diabetes in NOD mice associated with altered Mapk3 activities in B-lymphocytes

PLGA-microsphere delivery of insulin and IGRP epitopes as a therapy for type 1 diabetes

Nfkbid overexpression in NOD mice elicits complete type 1 diabetes resistance in part associated with enhanced thymic deletion of pathogenic CD8 T-cells and increased numbers and activity of regulatory T-cells.1,2,3

Nfkbid overexpression in NOD mice elicits complete type 1 diabetes resistance

HLA-B39:06 Efficiently Mediates Type 1 Diabetes in a Mouse Model Incorporating Reduced Thymic Insulin Expression1

Transient BAFF blockade inhibits type 1 diabetes development in NOD mice by enriching immunoregulatory B-lymphocytes sensitive to deletion by anti-CD20 co-therapy1, 2

T cells from NOD-PerIg mice target both pancreatic and neuronal tissue1,2

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