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Your search keyword '"Sather, Blythe D"' showing total 26 results
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26 results on '"Sather, Blythe D"'

1. γ-Secretase inhibitor in combination with BCMA chimeric antigen receptor T-cell immunotherapy for individuals with relapsed or refractory multiple myeloma: a phase 1, first-in-human trial

Author

Cowan, Andrew J, Pont, Margot J, Sather, Blythe D, Turtle, Cameron J, Till, Brian G, Libby, Edward N, 3rd, Coffey, David G, Tuazon, Sherilyn A, Wood, Brent, Gooley, Ted, Wu, Vicky Q, Voutsinas, Jenna, Song, Xiaoling, Shadman, Mazyar, Gauthier, Jordan, Chapuis, Aude G, Milano, Filippo, Maloney, David G, Riddell, Stanley R, and Green, Damian J

Published
2023
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2. CD8+ T Cell Tolerance to a Tumor-associated Antigen Is Maintained at the Level of Expansion Rather than Effector Function

Author

Öhlén, Claes, Kalos, Michael, Cheng, Laurence E, Shur, Aaron C, Hong, Doley J, Carson, Bryan D, Kokot, Niels CT, Lerner, Cara G, Sather, Blythe D, Huseby, Eric S, and Greenberg, Philip D

Subjects
Autoimmune Disease, Cancer, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, 5.2 Cellular and gene therapies, Aetiology, Inflammatory and immune system, Animals, Antigens, Neoplasm, CD8-Positive T-Lymphocytes, Calcium, Cell Division, Cell Extracts, Flow Cytometry, Gene Expression, Immune Tolerance, Interferon-gamma, Interleukin-2, JNK Mitogen-Activated Protein Kinases, Mice, Mice, Transgenic, Mitogen-Activated Protein Kinase Kinases, Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-bcl-2, Receptors, Antigen, T-Cell, Signal Transduction, Spleen, Tumor Necrosis Factor-alpha, fas Receptor, ras Proteins, CTL, hepatocyte, tumor immunology, autoimmunity, signaling, Medical and Health Sciences, Immunology
Abstract

CD8+ T cell tolerance to self-proteins prevents autoimmunity but represents an obstacle to generating T cell responses to tumor-associated antigens. We have made a T cell receptor (TCR) transgenic mouse specific for a tumor antigen and crossed TCR-TG mice to transgenic mice expressing the tumor antigen in hepatocytes (gag-TG). TCRxgag mice showed no signs of autoimmunity despite persistence of high avidity transgenic CD8+ T cells in the periphery. Peripheral CD8+ T cells expressed phenotypic markers consistent with antigen encounter in vivo and had upregulated the antiapoptotic molecule Bcl-2. TCRxgag cells failed to proliferate in response to antigen but demonstrated cytolytic activity and the ability to produce interferon gamma. This split tolerance was accompanied by inhibition of Ca(2+) flux, ERK1/2, and Jun kinase phosphorylation, and a block in both interleukin 2 production and response to exogenous interleukin 2. The data suggest that proliferation and expression of specific effector functions characteristic of reactive cells are not necessarily linked in CD8+ T cell tolerance.

Published
2002

5. Effective, safe, and sustained correction of murine XLA using a UCOE-BTK promoter-based lentiviral vector

Author

Seymour, Brenda J., primary, Singh, Swati, additional, Certo, Hannah M., additional, Sommer, Karen, additional, Sather, Blythe D., additional, Khim, Socheath, additional, Clough, Courtnee, additional, Hale, Malika, additional, Pangallo, Joseph, additional, Ryu, Byoung Y., additional, Khan, Iram F., additional, Adair, Jennifer E., additional, and Rawlings, David J., additional

Published
2021
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6. Interleukin-15 rescues tolerant CD8+ T cells for use in adoptive immunotherapy of established tumors

Author

Teague, Ryan M, Sather, Blythe D, Sacks, Jilian A, Huang, Maria Z, Dossett, Michelle L, Morimoto, Junko, Tan, Xiaoxio, Sutton, Susan E, Cooke, Michael P, Ohlen, Claes, and Greenberg, Philip D

Abstract

Author(s): Ryan M Teague [1, 2]; Blythe D Sather [1]; Jilian A Sacks [1]; Maria Z Huang [1]; Michelle L Dossett [1, 2]; Junko Morimoto [1, 2]; Xiaoxio Tan [1, [...]

Published
2006
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7. Abstract A027: Targeted insertion of an HPV-16 E7-specific engineered T-cell receptor into the TRAC locus

Author

Croft, Alexandra, primary, Brandt, Cameron, additional, Burleigh, Stephen, additional, Chadwick, Eric, additional, Chin, Melissa, additional, Toy, Dean, additional, Donahue, Bailey, additional, Patton, Clay, additional, Goldfless, Stephen, additional, Belmont, Brian, additional, Salmon, Ruth, additional, Welstead, Grant, additional, Sather, Blythe D., additional, and Huss, David J., additional

Published
2019
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8. 572. Successful Generation of CAR+PD-1-Primary T Cells Using Cas9-Mediated Genome Editing

Author

Welstead, Grant, primary, Fang, Justin, additional, Nye, Chris, additional, Buquicchio, Frank, additional, Collins, McKensie, additional, Selleck, Will, additional, Jayaram, Hari, additional, Salmon, Ruth, additional, Baturevych, Alex, additional, Mudri, Sherri, additional, Jones, Jon, additional, Bumcrot, David, additional, and Sather, Blythe D., additional

Published
2016
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9. Efficient Modification of the CCR5 Locus in Primary Human T Cells With megaTAL Nuclease Establishes HIV-1 Resistance

Author

Romano Ibarra, Guillermo S, primary, Paul, Biswajit, additional, Sather, Blythe D, additional, Younan, Patrick M, additional, Sommer, Karen, additional, Kowalski, John P, additional, Hale, Malika, additional, Stoddard, Barry, additional, Jarjour, Jordan, additional, Astrakhan, Alexander, additional, Kiem, Hans-Peter, additional, and Rawlings, David J, additional

Published
2016
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10. Cellular requirements for diabetes induction in DO11.10xRIPmOVA mice1

Author

Wesley, Johnna D., Sather, Blythe D., Perdue, Nikole, Ziegler, Steven, and Campbell, Daniel J.

Subjects
CD4-Positive T-Lymphocytes, B-Lymphocytes, Mice, Inbred BALB C, Ovalbumin, Histocompatibility Antigens Class II, Fluorescent Antibody Technique, Cell Differentiation, Enzyme-Linked Immunosorbent Assay, Mice, Transgenic, Cell Separation, CD8-Positive T-Lymphocytes, Flow Cytometry, Lymphocyte Activation, Adoptive Transfer, Immunohistochemistry, Article, Rats, Mice, Diabetes Mellitus, Type 1, T-Lymphocyte Subsets, Animals, Insulin, Promoter Regions, Genetic
Abstract

Type 1 Diabetes (T1D3) results from the immune-mediated destruction of the insulin producing β-islet cells in the pancreas. The genetic and environmental mechanisms promoting the development of this disease remain poorly understood. We have explored the cellular requirements for T1D development in DO11.10xRIP-OVA (DORmO) mice, which carry a T cell receptor transgene specific for an MHC class II-restricted epitope from ovalbumin (OVA) and express membrane-bound OVA in the pancreas under the control of the rat insulin promoter. We found that DORmO.RAG2−/− mice do not develop insulitis and are completely protected from diabetes, demonstrating that endogenous lymphocyte receptor rearrangement is required for disease development. Diabetes in DORmO mice is preceded by the development of OVA-specific autoantibodies, and is delayed in B cell-deficient DORmO.JHD−/− mice, demonstrating that B cells contribute to disease progression. In addition, transfer of CD8+ T cells from diabetic animals into DORmO.RAG2−/− mice promoted insulitis by OVA-specific CD4+ T cells. Finally, although diabetes develops in DORmO mice in the presence of a significant population of Foxp3+ OVA-specific regulatory T cells, boosting regulatory T cell numbers by injecting IL-2 immune complexes dampens autoantibody production and prevents development of insulitis and overt diabetes. These results help define the events leading to diabetes in DORmO mice, and provide new insights into the cellular interactions required for disease development in an antigen-specific model of T1D.

Published
2010

11. Efficient modification of CCR5 in primary human hematopoietic cells using a megaTAL nuclease and AAV donor template

Author

Sather, Blythe D., primary, Romano Ibarra, Guillermo S., additional, Sommer, Karen, additional, Curinga, Gabrielle, additional, Hale, Malika, additional, Khan, Iram F., additional, Singh, Swati, additional, Song, Yumei, additional, Gwiazda, Kamila, additional, Sahni, Jaya, additional, Jarjour, Jordan, additional, Astrakhan, Alexander, additional, Wagner, Thor A., additional, Scharenberg, Andrew M., additional, and Rawlings, David J., additional

Published
2015
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13. 685. Efficient Targeted Gene Modification in Primary Human Hematopoietic Cells Using Co-Delivery of Nuclease mRNA and AAV Donors

Author

Romano Ibarra, Guillermo S., primary, Curinga, Gabrielle, additional, Sather, Blythe D., additional, Sommer, Karen M., additional, Hale, Malika, additional, Khan, Iram, additional, Singh, Swati, additional, Song, Youmei, additional, Gwiazda, Kamila, additional, Sahni, Jaya, additional, Khim, Socheath, additional, Astrakhan, Alexander, additional, Wagner, Thor, additional, Scharenberg, Andrew M., additional, and Rawlings, David J., additional

Published
2015
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14. Rapamycin relieves lentiviral vector transduction resistance in human and mouse hematopoietic stem cells

Author

Wang, Cathy X., primary, Sather, Blythe D., additional, Wang, Xuefeng, additional, Adair, Jennifer, additional, Khan, Iram, additional, Singh, Swati, additional, Lang, Shanshan, additional, Adams, Amie, additional, Curinga, Gabrielle, additional, Kiem, Hans-Peter, additional, Miao, Carol H., additional, Rawlings, David J., additional, and Torbett, Bruce E., additional

Published
2014
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15. Trypanosoma cruzi trans-sialidase initiates a program independent of the transcription factors RORγt and Ahr that leads to IL-17 production by activated B cells

Author

Bermejo, Daniela A, primary, Jackson, Shaun W, additional, Gorosito-Serran, Melisa, additional, Acosta-Rodriguez, Eva V, additional, Amezcua-Vesely, Maria C, additional, Sather, Blythe D, additional, Singh, Akhilesh K, additional, Khim, Socheath, additional, Mucci, Juan, additional, Liggitt, Denny, additional, Campetella, Oscar, additional, Oukka, Mohamed, additional, Gruppi, Adriana, additional, and Rawlings, David J, additional

Published
2013
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16. WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity

Author

Becker-Herman, Shirly, primary, Meyer-Bahlburg, Almut, additional, Schwartz, Marc A., additional, Jackson, Shaun W., additional, Hudkins, Kelly L., additional, Liu, Chaohong, additional, Sather, Blythe D., additional, Khim, Socheath, additional, Liggitt, Denny, additional, Song, Wenxia, additional, Silverman, Gregg J., additional, Alpers, Charles E., additional, and Rawlings, David J., additional

Published
2011
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23. Interleukin-15 rescues tolerant CD8+ T cells for use in adoptive immunotherapy of established tumors.

Author

Teague, Ryan M., Sather, Blythe D., Sacks, Jilian A., Huang, Maria Z., Dossett, Michelle L., Morimoto, Junko, Xiaoxio Tan, Sutton, Susan E., Cooke, Michael P., Öhlén, Claes, and Greenberg, Philip D.

Subjects
*T cell differentiation, *CANCER cell growth, *TUMOR antigens, *IMMUNIZATION, *IMMUNE recognition, *TUMOR treatment
Abstract

CD8+ T cells can mediate eradication of established tumors, and strategies to amplify tumor-reactive T-cell numbers by immunization or ex vivo expansion followed by adoptive transfer are currently being explored in individuals with cancer. Generating effective CD8+ T cell–mediated responses to tumors is often impeded by T-cell tolerance to relevant tumor antigens, as most of these antigens are also expressed in normal tissues. We examined whether such tolerant T cells could be rescued and functionally restored for use in therapy of established tumors. We used a transgenic T-cell receptor (TCR) mouse model in which peripheral CD8+ T cells specific for a candidate tumor antigen also expressed in liver are tolerant, failing to proliferate or secrete interleukin (IL)-2 in response to antigen. Molecular and cellular analysis showed that these tolerant T cells expressed the IL-15 receptor α chain, and could be induced to proliferate in vitro in response to exogenous IL-15. Such proliferation abrogated tolerance and the rescued cells became effective in treating leukemia. Therefore, high-affinity CD8+ T cells are not necessarily deleted by encounter with self-antigen in the periphery, and can potentially be rescued and expanded for use in tumor immunotherapy. [ABSTRACT FROM AUTHOR]

Published
2006
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25. Efficient modification of CCR5in primary human hematopoietic cells using a megaTAL nuclease and AAV donor template

Author

Sather, Blythe D., Romano Ibarra, Guillermo S., Sommer, Karen, Curinga, Gabrielle, Hale, Malika, Khan, Iram F., Singh, Swati, Song, Yumei, Gwiazda, Kamila, Sahni, Jaya, Jarjour, Jordan, Astrakhan, Alexander, Wagner, Thor A., Scharenberg, Andrew M., and Rawlings, David J.

Abstract

Therapeutic coding sequences can be targeted to the CCR5locus of primary human T cells with high efficiency by using megaTAL nuclease and an AAV donor template.

Published
2015
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26. WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

Author

Becker-Herman S, Meyer-Bahlburg A, Schwartz MA, Jackson SW, Hudkins KL, Liu C, Sather BD, Khim S, Liggitt D, Song W, Silverman GJ, Alpers CE, and Rawlings DJ

Subjects
Animals, Antibodies, Antinuclear immunology, Autoantibodies immunology, B-Lymphocytes physiology, CD4-Positive T-Lymphocytes immunology, Chimera, Female, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Myeloid Differentiation Factor 88 immunology, Receptors, Antigen, B-Cell immunology, Toll-Like Receptors immunology, Wiskott-Aldrich Syndrome Protein genetics, Autoimmunity immunology, B-Lymphocytes immunology, Wiskott-Aldrich Syndrome Protein deficiency
Abstract

Patients with the immunodeficiency Wiskott-Aldrich syndrome (WAS) frequently develop systemic autoimmunity. Here, we demonstrate that mutation of the WAS gene results in B cells that are hyperresponsive to B cell receptor and Toll-like receptor (TLR) signals in vitro, thereby promoting a B cell-intrinsic break in tolerance. Whereas this defect leads to autoantibody production in WAS protein-deficient (WASp(-/-)) mice without overt disease, chimeric mice in which only the B cell lineage lacks WASp exhibit severe autoimmunity characterized by spontaneous germinal center formation, class-switched autoantibodies, renal histopathology, and early mortality. Both T cell help and B cell-intrinsic TLR engagement play important roles in promoting disease in this model, as depletion with anti-CD4 antibodies or generation of chimeric mice with B cells deficient in both WASp and MyD88 prevented development of autoimmune disease. These data highlight the potentially harmful role for cell-intrinsic loss of B cell tolerance in the setting of normal T cell function, and may explain why WAS patients with mixed chimerism after stem cell transplantation often develop severe humoral autoimmunity.

Published
2011
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