ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Activation receptor-induced tolerance of mature NK cells in vivo requires signaling through the receptor and is reversible.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Single-cell transcriptomics identifies altered neutrophil dynamics and accentuated T-cell cytotoxicity in tobacco flavored e-cigarette exposed mouse lungs.bioRxiv : the preprint server for biology · 2025Article
- Outsmarting trogocytosis to boost CAR NK/T cell therapy.Molecular cancer · 2023Review
- Activation Receptor-Dependent IFN-γ Production by NK Cells Is Controlled by Transcription, Translation, and the Proteasome.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- NK Cell Hyporesponsiveness: More Is Not Always Better.International journal of molecular sciences · 2019Review
- Enhanced adaptive immune responses in lung adenocarcinoma through natural killer cell stimulation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Chronic Ly49H Receptor EngagementFrontiers in immunology · 2019Article
- Expression of the inhibitory receptor NKG2A correlates with increased liver and splenic NK cell response to activating receptor engagement.Immunity, inflammation and disease · 2017Article
- The role of NK cells in HIV-1 protection: autologous, allogeneic or both?AIDS research and therapy · 2016Review
- Prenatal Allospecific NK Cell Tolerance Hinges on Instructive Allorecognition through the Activating Receptor during Development.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Acquisition of activation receptor ligand by trogocytosis renders NK cells hyporesponsive.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Activating killer cell Ig-like receptors in health and disease.Frontiers in immunology · 2014Review
- Viral infection transiently reverses activation receptor-mediated NK cell hyporesponsiveness in an MHC class I-independent mechanism.European journal of immunology · 2013Article
- Natural killer cell functional dichotomy: a feature of chronic viral hepatitis?Frontiers in immunology · 2012Article
- Unifying concepts of MHC-dependent natural killer cell education.Trends in immunology · 2011Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
NK cell responses are determined by signals received through activating and inhibitory cell surface receptors. Ly49H is an NK cell-specific activating receptor that accounts for the genetic resistance to murine CMV (MCMV). The Ly49H receptor has been shown to interact with two adaptor proteins (DAP12 and DAP10). In the context of MCMV infection, interaction of m157 (the MCMV-encoded ligand for Ly49H) with Ly49H results in activation of Ly49H-expressing NK cells. Chronic exposure of Ly49H with m157, however, induces tolerance in these same cells. The mechanism of this tolerance remains poorly understood. Using a transgenic mouse model, we demonstrate that induction of tolerance in Ly49H(+) NK cells by chronic exposure to m157, in vivo, requires signaling through the Ly49H adaptor protein DAP12, but not the DAP10 adaptor protein. Furthermore, mature Ly49H-expressing NK cells from wild-type mice can acquire a tolerant phenotype by 24 h posttransfer into a transgenic C57BL/6 mouse that expresses m157. The tolerant phenotype can be reversed, in vivo, if tolerant NK cells are transferred to mice that do not express the m157 protein. Thus, continuous activating receptor engagement can induce a transient tolerance in mature NK cells in vivo. These observations provide new insight into how activating receptor engagement shapes NK cell function and has important implications in how NK cells respond to tumors and during chronic viral infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.