J. Katz

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Bcl-2 Allows Effector and Memory CD8+ T Cells To Tolerate Higher Expression of Bim

H. Grimes, David A Hildeman, S. Kurtulus, 2011, The Journal of Immunology.

Cells To Tolerate Higher Expression of Bim T + Bcl-2 Allows Effector and Memory CD8

H. Grimes, David A Hildeman, S. Kurtulus, 2011 .

Islet-specific T-cell clones from nonobese diabetic mice express heterogeneous T-cell receptors.

C. Benoist, D. Mathis, J. Katz, 1991, Proceedings of the National Academy of Sciences of the United States of America.

In Autoimmune Diabetes the Transition from Benign to Pernicious Insulitis Requires an Islet Cell Response to Tumor Necrosis Factor α

J. Katz, S. Pakala, M. Chivetta, 1999, The Journal of experimental medicine.

Genetic Control of Diabetes Progression the islets ; after a substantial delay , destruction of the

M. Mattei, H. Kikutani, J. Katz, 1997 .

Microarray and comparative genomics-based identification of genes and gene regulatory regions of the mouse immune system

Sue Kong, Bruce J Aronow, Anil G Jegga, 2004, BMC Genomics.

NKT Cells and IFN-γ Establish the Regulatory Environment for the Control of Diabetogenic T Cells in the Nonobese Diabetic Mouse1

J. Katz, Judith A. Smith, Jennifer K. Ondr, 2006, The Journal of Immunology.

CD8+ T cells specific for β cells encounter their cognate antigens in the islets of NOD mice

R. Tisch, Jiajun Zhao, J. Katz, 2009, European journal of immunology.

Breaking T cell tolerance to beta cell antigens by merocytic dendritic cells

J. Katz, E. Janssen, 2011, Cellular and Molecular Life Sciences.

Checkpoints in the progression of autoimmune disease: lessons from diabetes models.

C. Benoist, D. Mathis, J. Katz, 1996, Proceedings of the National Academy of Sciences of the United States of America.

Expression of Diabetes-Associated Genes by Dendritic Cells and CD4 T Cells Drives the Loss of Tolerance in Nonobese Diabetic Mice1

L. Wen, M. Shlomchik, J. Katz, 2009, The Journal of Immunology.

Loss of Tolerance in Nonobese Diabetic Mice Dendritic Cells and CD4 T Cells Drives the Expression of Diabetes-Associated Genes by

M. Shlomchik, J. Katz, L. Wicker, 2009 .

Regulation of autoimmune diabetes by non‐islet‐specific T cells — a role for the glucocorticoid‐induced TNF receptor

E. Unanue, J. Katz, J. Shimizu, 2004, European journal of immunology.

Major Histocompatibility Complex Class II Molecules Can Protect from Diabetes by Positively Selecting T Cells with Additional Specificities

C. Benoist, D. Mathis, J. Katz, 1998, The Journal of experimental medicine.

Bim/Bcl-2 balance is critical for maintaining naive and memory T cell homeostasis

F. Finkelman, H. Grimes, David A Hildeman, 2007, The Journal of experimental medicine.

Diabetesin Nonobese Diabetic Mouse Cells Break T Cell Tolerance to ² Cell Cutting Edge: Merocytic Dendritic

Robert Opoka, J. Katz, E. Janssen, 2010 .

Cutting Edge: Merocytic Dendritic Cells Break T Cell Tolerance to β Cell Antigens in Nonobese Diabetic Mouse Diabetes

Robert Opoka, J. Katz, E. Janssen, 2010, The Journal of Immunology.

Dynamic interaction between T cell-mediated β-cell damage and β-cell repair in the run up to autoimmune diabetes of the NOD mouse

B. Aronow, A. Jegga, J. Hutton, 2005 .

Beta cell apoptosis in T cell-mediated autoimmune diabetes.

M. Kurrer, J. Katz, S. Pakala, 1997, Proceedings of the National Academy of Sciences of the United States of America.

IFN- γ receptor deficiency prevents diabetes induction by diabetogenic CD4 + T cells but not CD8 + T cells 1

J. Katz, Alaina L. Garland, Li Li, 2014 .

Transgenic mice carrying the rearranged T cell receptor of a diabetogenic T cell clone

C. Benoist, D. Mathis, J. Katz, 1994 .

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

C. Benoist, D. Mathis, J. Katz, 1993, European journal of immunology.

Interleukin-4 Deficiency Does Not Exacerbate Disease in NOD Mice

C. Benoist, D. Mathis, J. Katz, 1998, Diabetes.

Autoimmune Diabetes in the Nonobese Plasmacytoid Dendritic Cells Control The Countervailing Actions of Myeloid and

J. Katz, A. Magnusen, V. Saxena, 2012 .

The Countervailing Actions of Myeloid and Plasmacytoid Dendritic Cells Control Autoimmune Diabetes in the Nonobese Diabetic Mouse1

D. Munn, J. Katz, A. Magnusen, 2007, The Journal of Immunology.

Mechanism of defective NK cell activity in patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex. I. Defective trigger on NK cells for NKCF production by target cells, and partial restoration by IL 2.

M. Gottlieb, J. Katz, B. Bonavida, 1986, Journal of immunology.

Etoposide Selectively Ablates Activated T Cells To Control the Immunoregulatory Disorder Hemophagocytic Lymphohistiocytosis

David A Hildeman, J. Katz, M. Jordan, 2014, The Journal of Immunology.

IL-10 deficiency does not inhibit insulitis and accelerates cyclophosphamide-induced diabetes in the nonobese diabetic mouse.

N. Sarvetnick, J. Katz, B. Balasa, 2000, Cellular immunology.

Mechanism of defective NK cell activity in patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex. II. Normal antibody-dependent cellular cytotoxicity (ADCC) mediated by effector cells defective in natural killer (NK) cytotoxicity.

M. Gottlieb, J. Katz, B. Bonavida, 1987, Journal of immunology.

Following a diabetogenic T cell from genesis through pathogenesis

C. Benoist, D. Mathis, J. Katz, 1993, Cell.

Cutting Edge: Thymic Positive Selection and Peripheral Activation of Islet Antigen-Specific T Cells: Separation of Two Diabetogenic Steps by an I-Ag7 Class II MHC β-Chain Mutant

E. Unanue, J. Katz, O. Kanagawa, 1998, The Journal of Immunology.

This information is current as Lymphohistiocytosis Disorder Hemophagocytic Cells To Control the Immunoregulatory Etoposide Selectively Ablates Activated T

David A Hildeman, J. Katz, M. Jordan, 2013 .

A spontaneous sarcoma dependent on host tumor‐specific immune lymphocytes

J. Katz, B. Bonavida, 1989, BioEssays : news and reviews in molecular, cellular and developmental biology.

The SJL/J T cell response to both spontaneous and transplantable syngeneic reticulum cell sarcoma is mediated predominantly by the V beta 17a+ T cell clonotype

J. Katz, B. Bonavida, K. Ohnishi, 1988, The Journal of experimental medicine.

Restoring tolerance to β-cells in Type 1 diabetes: Current and emerging strategies.

J. Katz, Kaitlin R Carroll, 2022, Cellular immunology.

Mechanism of T-dependent cytotoxicity: role of papain-sensitive non class I MHC target molecules and expression of target antigen for cytotoxicity.

J. Katz, H. Ostergaard, B. Bonavida, 1985, Advances in experimental medicine and biology.

The in vivo depletion of V beta 17a+ T cells results in the inhibition of reticulum cell sarcoma growth in SJL/J mice. Evidence for the use of anticlonotypic antibody therapy in the control of malignancy.

J. Katz, B. Bonavida, L. Lebow, 1989, Journal of immunology.

T helper cell subsets in insulin-dependent diabetes.

C Benoist, C. Benoist, D. Mathis, 1995, Science.

Humoral and T-cell responses to SARS-CoV-2 vaccination in multiple sclerosis patients treated with ocrelizumab

J. Katz, E. Lathi, A. Bouley, 2021, Multiple Sclerosis and Related Disorders.

Mechanism of NK activation by OK-432 (Streptococcus pyogenes). I. Spontaneous release of NKCF and augmentation of NKCF production following stimulation with NK target cells.

J. Katz, B. Bonavida, T. Hoshino, 1986, Cellular immunology.

The Murine Gammaherpesvirus 68 v-Cyclin Gene Is an Oncogene That Promotes Cell Cycle Progression in Primary Lymphocytes

J. Hess, H. Virgin, J. Katz, 1999, Journal of Virology.

Dying to protect: cell death and the control of T‐cell homeostasis

David A Hildeman, J. Katz, M. Jordan, 2017, Immunological reviews.

T cells instruct myeloid cells to produce inflammasome-independent IL-1β and cause autoimmunity

A. Chervonsky, A. Oberst, J. Katz, 2019, Nature Immunology.

IFN‐γ receptor deficiency prevents diabetes induction by diabetogenic CD4+, but not CD8+, T cells

Li Li, Bo Wang, R. Tisch, 2012, European journal of immunology.

Interferon-gamma impacts at multiple points during the progression of autoimmune diabetes.

C. Benoist, D. Mathis, J. Katz, 1997, Proceedings of the National Academy of Sciences of the United States of America.

Undermining Protective Immunity Eliminating Encephalitogenic T Cells without

David A Hildeman, J. Katz, M. Jordan, 2017 .

Eliminating Encephalitogenic T Cells without Undermining Protective Immunity

David A Hildeman, J. Katz, M. Jordan, 2014, The Journal of Immunology.

T Helper 2 (Th2) T Cells Induce Acute Pancreatitis and Diabetes in Immune-compromised Nonobese Diabetic (NOD) Mice

M. Kurrer, J. Katz, S. Pakala, 1997, The Journal of experimental medicine.

Manipulating DNA damage-response signaling for the treatment of immune-mediated diseases

Michael M. Henry, M. Hermiston, P. Andreassen, 2017, Proceedings of the National Academy of Sciences.

T cells instruct dendritic cells to produce inflammasome independent IL-1β causing systemic inflammation

A. Chervonsky, A. Oberst, J. Katz, 2018, bioRxiv.

Reversal of New-Onset Type 1 Diabetes With an Agonistic TLR4/MD-2 Monoclonal Antibody

J. Katz, H. Tsukamoto, S. Ohta, 2015, Diabetes.

Extending Remission and Reversing New-Onset Type 1 Diabetes by Targeted Ablation of Autoreactive T Cells

David A Hildeman, J. Katz, M. Jordan, 2018, Diabetes.

The Murine Gammaherpesvirus 68 v-Cyclin Gene Is an Oncogene That Promotes Cell Cycle Progression in Primary Lymphocytes

J. Hess, H. Virgin, J. Katz, 1999, Journal of Virology.

Pro-Inflammatory Alterations of Circulating Monocytes in Latent Tuberculosis Infection

C. Fichtenbaum, Sandra Andorf, C. D. De Cecco, 2022, Open forum infectious diseases.

Erratum: The murine gammaherpesvirus 68 v-cyclin gene is an oncogene that promotes cell cycle progression in primary lymphocytes (Journal of Virology (1999) 73:6 (5110-5122))

J. Hess, H. Virgin, J. Katz, 1999 .

Subset-specific and temporal control of effector and memory CD4+ T cell survival

David A Hildeman, J. Katz, M. Herold, 2023, bioRxiv.

T cells instruct myeloid cells to produce inflammasome-independent IL-1β and cause autoimmunity

A. Chervonsky, A. Oberst, J. Katz, 2019, Nature Immunology.

Thymic positive selection and peripheral activation of islet antigen-specific T cells: separation of two diabetogenic steps by an I-A(g7) class II MHC beta-chain mutant.

E. Unanue, J. Katz, O. Kanagawa, 1998, Journal of immunology.

Adaptation of Imaging Mass Cytometry to Explore the Single Cell Alloimmune Landscape of Liver Transplant Rejection

S. Asgharzadeh, J. Katz, Naim Matasci, 2022, Frontiers in Immunology.

Dying to protect: cell death and the control of T‐cell homeostasis

David A Hildeman, J. Katz, M. Jordan, 2017, Immunological reviews.

Nonobese Diabetic Mouse Diabetes Cell Antigens in b Break T Cell Tolerance to Cutting Edge: Merocytic Dendritic Cells

Jonathan D. Katz, Robert Opoka, J. Katz, 2010 .

Dynamic interaction between T cell-mediated beta-cell damage and beta-cell repair in the run up to autoimmune diabetes of the NOD mouse.

B. Aronow, A. Jegga, J. Hutton, 2005, Physiological genomics.

CD8+ T cells specific for β cells encounter their cognate antigens in the islets of NOD mice

R. Tisch, Jiajun Zhao, J. Katz, 2009, European journal of immunology.

Studies on the induction and expression of T cell-mediated immunity. XV. Role of non-MHC papain-sensitive target structures and Lyt-2 antigens in allogeneic and xenogeneic lectin-dependent cellular cytotoxicity (LDCC).

J. Katz, B. Bonavida, 1974, Journal of immunology.

Interleukin-4 Deficiency Does Not Exacerbate Disease in NOD Mice

C. Benoist, D. Mathis, J. Katz, 1998, Diabetes.