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Your search keyword '"Murphy, Kenneth M."' showing total 22 results
Start Over Author "Murphy, Kenneth M." Journal journal of experimental medicine
22 results on '"Murphy, Kenneth M."'

1. IL-6 selectively suppresses cDC1 specification via C/EBPβ

Author

Kim, Sunkyung, primary, Chen, Jing, additional, Jo, Suin, additional, Ou, Feiya, additional, Ferris, Stephen T., additional, Liu, Tian-Tian, additional, Ohara, Ray A., additional, Anderson, David A., additional, Wu, Renee, additional, Chen, Michael Y., additional, Gillanders, William E., additional, Murphy, Theresa L., additional, and Murphy, Kenneth M., additional

Published
2023
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2. A crucial role for HVEM and BTLA in preventing intestinal inflammation

Author

Steinberg, Marcos W, Turovskaya, Olga, Shaikh, Raziya B, Kim, Gisen, McCole, Declan F, Pfeffer, Klaus, Murphy, Kenneth M, Ware, Carl F, and Kronenberg, Mitchell

Subjects
Autoimmune Disease, Inflammatory Bowel Disease, Digestive Diseases, Prevention, Aetiology, 2.1 Biological and endogenous factors, Animals, B-Lymphocytes, CD4-Positive T-Lymphocytes, Colitis, Homeodomain Proteins, Inflammation, Lymphocyte Depletion, Mice, Mice, Knockout, Receptors, Immunologic, Receptors, Tumor Necrosis Factor, Member 14, T-Lymphocytes, T-Lymphocytes, Regulatory, Medical and Health Sciences, Immunology
Abstract

The interaction between the tumor necrosis factor (TNF) family member LIGHT and the TNF family receptor herpes virus entry mediator (HVEM) co-stimulates T cells and promotes inflammation. However, HVEM also triggers inhibitory signals by acting as a ligand that binds to B and T lymphocyte attenuator (BTLA), an immunoglobulin super family member. The contribution of HVEM interacting with these two binding partners in inflammatory processes remains unknown. In this study, we investigated the role of HVEM in the development of colitis induced by the transfer of CD4(+)CD45RB(high) T cells into recombination activating gene (Rag)(-/-) mice. Although the absence of HVEM on the donor T cells led to a slight decrease in pathogenesis, surprisingly, the absence of HVEM in the Rag(-/-) recipients led to the opposite effect, a dramatic acceleration of intestinal inflammation. Furthermore, the critical role of HVEM in preventing colitis acceleration mainly involved HVEM expression by radioresistant cells in the Rag(-/-) recipients interacting with BTLA. Our experiments emphasize the antiinflammatory role of HVEM and the importance of HVEM expression by innate immune cells in preventing runaway inflammation in the intestine.

Published
2008

8. RAG-mediated DNA double-strand breaks activate a cell type–specific checkpoint to inhibit pre–B cell receptor signals

Author

Bednarski, Jeffrey J., primary, Pandey, Ruchi, additional, Schulte, Emily, additional, White, Lynn S., additional, Chen, Bo-Ruei, additional, Sandoval, Gabriel J., additional, Kohyama, Masako, additional, Haldar, Malay, additional, Nickless, Andrew, additional, Trott, Amanda, additional, Cheng, Genhong, additional, Murphy, Kenneth M., additional, Bassing, Craig H., additional, Payton, Jacqueline E., additional, and Sleckman, Barry P., additional

Published
2016
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9. Migratory CD103+ dendritic cells suppress helminth-driven type 2 immunity through constitutive expression of IL-12

Author

Everts, Bart, primary, Tussiwand, Roxane, additional, Dreesen, Leentje, additional, Fairfax, Keke C., additional, Huang, Stanley Ching-Cheng, additional, Smith, Amber M., additional, O’Neill, Christina M., additional, Lam, Wing Y., additional, Edelson, Brian T., additional, Urban, Joseph F., additional, Murphy, Kenneth M., additional, and Pearce, Edward J., additional

Published
2015
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11. CRTAM controls residency of gut CD4+CD8+ T cells in the steady state and maintenance of gut CD4+ Th17 during parasitic infection

Author

Cortez, Victor S., primary, Cervantes-Barragan, Luisa, additional, Song, Christina, additional, Gilfillan, Susan, additional, McDonald, Keely G., additional, Tussiwand, Roxane, additional, Edelson, Brian T., additional, Murakami, Yoshinori, additional, Murphy, Kenneth M., additional, Newberry, Rodney D., additional, Sibley, L. David, additional, and Colonna, Marco, additional

Published
2014
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13. Type I interferon is selectively required by dendritic cells for immune rejection of tumors

Author

Diamond, Mark S., primary, Kinder, Michelle, additional, Matsushita, Hirokazu, additional, Mashayekhi, Mona, additional, Dunn, Gavin P., additional, Archambault, Jessica M., additional, Lee, Hsiaoju, additional, Arthur, Cora D., additional, White, J. Michael, additional, Kalinke, Ulrich, additional, Murphy, Kenneth M., additional, and Schreiber, Robert D., additional

Published
2011
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15. Targeting of B and T lymphocyte associated (BTLA) prevents graft-versus-host disease without global immunosuppression

Author

Albring, Jörn C., primary, Sandau, Michelle M., additional, Rapaport, Aaron S., additional, Edelson, Brian T., additional, Satpathy, Ansuman, additional, Mashayekhi, Mona, additional, Lathrop, Stephanie K., additional, Hsieh, Chyi-Song, additional, Stelljes, Matthias, additional, Colonna, Marco, additional, Murphy, Theresa L., additional, and Murphy, Kenneth M., additional

Published
2010
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16. Peripheral CD103+ dendritic cells form a unified subset developmentally related to CD8α+ conventional dendritic cells

Author

Edelson, Brian T., primary, KC, Wumesh, additional, Juang, Richard, additional, Kohyama, Masako, additional, Benoit, Loralyn A., additional, Klekotka, Paul A., additional, Moon, Clara, additional, Albring, Jörn C., additional, Ise, Wataru, additional, Michael, Drew G., additional, Bhattacharya, Deepta, additional, Stappenbeck, Thaddeus S., additional, Holtzman, Michael J., additional, Sung, Sun-Sang J., additional, Murphy, Theresa L., additional, Hildner, Kai, additional, and Murphy, Kenneth M., additional

Published
2010
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21. Transition from cMyc to L-Myc during dendritic cell development coordinated by rising levels of IRF8.

Author

Anderson DA, Ou F, Kim S, Murphy TL, and Murphy KM

Subjects
Animals, Cell Cycle Proteins genetics, Enhancer Elements, Genetic, Genes, Reporter, Immunophenotyping, Interferon Regulatory Factors metabolism, Lymphoid Progenitor Cells cytology, Lymphoid Progenitor Cells immunology, Lymphoid Progenitor Cells metabolism, Mice, Mice, Knockout, Protein Binding, Proto-Oncogene Proteins metabolism, Trans-Activators metabolism, Cell Differentiation genetics, Dendritic Cells cytology, Dendritic Cells metabolism, Gene Expression Regulation, Genes, myc, Interferon Regulatory Factors genetics
Abstract

During dendritic cell (DC) development, Myc expression in progenitors is replaced by Mycl in mature DCs, but when and how this transition occurs is unknown. We evaluated DC development using reporters for MYC, MYCL, and cell cycle proteins Geminin and CDT1 in wild-type and various mutant mice. For classical type 1 dendritic cells (cDC1s) and plasmacytoid DCs (pDCs), the transition occurred upon their initial specification from common dendritic cell progenitors (CDPs) or common lymphoid progenitors (CLPs), respectively. This transition required high levels of IRF8 and interaction with PU.1, suggesting the use of EICEs within Mycl enhancers. In pDCs, maximal MYCL induction also required the +41kb Irf8 enhancer that controls pDC IRF8 expression. IRF8 also contributed to repression of MYC. While MYC is expressed only in rapidly dividing DC progenitors, MYCL is most highly expressed in DCs that have exited the cell cycle. Thus, IRF8 levels coordinate the Myc-Mycl transition during DC development., Competing Interests: Disclosures: The authors declare no competing interests exist., (© 2021 Anderson et al.)

Published
2022
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22. Migratory CD103+ dendritic cells suppress helminth-driven type 2 immunity through constitutive expression of IL-12.

Author

Everts B, Tussiwand R, Dreesen L, Fairfax KC, Huang SC, Smith AM, O'Neill CM, Lam WY, Edelson BT, Urban JF Jr, Murphy KM, and Pearce EJ

Subjects
Animals, Basic-Leucine Zipper Transcription Factors deficiency, Basic-Leucine Zipper Transcription Factors genetics, Basic-Leucine Zipper Transcription Factors metabolism, Cell Movement, Disease Resistance immunology, Female, Helminthiasis genetics, Helminthiasis immunology, Helminthiasis metabolism, Immunization, Interleukin-12 biosynthesis, Liver Cirrhosis etiology, Liver Cirrhosis pathology, Mice, Mice, Knockout, Models, Animal, Repressor Proteins deficiency, Repressor Proteins genetics, Repressor Proteins metabolism, Th2 Cells immunology, Th2 Cells metabolism, Toll-Like Receptors metabolism, Antigens, CD metabolism, Dendritic Cells immunology, Dendritic Cells metabolism, Gene Expression Regulation, Helminths immunology, Immunity genetics, Immunomodulation, Integrin alpha Chains metabolism, Interleukin-12 genetics
Abstract

CD8α(+) and CD103(+) dendritic cells (DCs) play a central role in the development of type 1 immune responses. However, their role in type 2 immunity remains unclear. We examined this issue using Batf3(-/-) mice, in which both of these DC subsets are missing. We found that Th2 cell responses, and related events such as eosinophilia, alternative macrophage activation, and immunoglobulin class switching to IgG1, were enhanced in Batf3(-/-) mice responding to helminth parasites. This had beneficial or detrimental consequences depending on the context. For example, Batf3 deficiency converted a normally chronic intestinal infection with Heligmosomoides polygyrus into an infection that was rapidly controlled. However, liver fibrosis, an IL-13-mediated pathological consequence of wound healing in chronic schistosomiasis, was exacerbated in Batf3(-/-) mice infected with Schistosoma mansoni. Mechanistically, steady-state production of IL-12 by migratory CD103(+) DCs, independent of signals from commensals or TLR-initiated events, was necessary and sufficient to exert the suppressive effects on Th2 response development. These findings identify a previously unrecognized role for migratory CD103(+) DCs in antagonizing type 2 immune responses., (© 2016 Everts et al.)

Published
2016
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