ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Ly49-dependent NK cell licensing and effector inhibition involve the same interaction site on MHC ligands.
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 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Expression of a single inhibitory member of the Ly49 receptor family is sufficient to license NK cells for effector functions.bioRxiv : the preprint server for biology · 2024Article
- IL27 Signaling Serves as an Immunologic Checkpoint for Innate Cytotoxic Cells to Promote Hepatocellular Carcinoma.Cancer discovery · 2022Article
- Control of Viral Infection by Natural Killer Cell Inhibitory Receptors.Cell reports · 2020Article
- Functional Characterization of Ly49Frontiers in immunology · 2020Article
- Synergized regulation of NK cell education by NKG2A and specific Ly49 family members.Nature communications · 2019Article
- Immunoreceptor tyrosine-based inhibitory motif-dependent functions of an MHC class I-specific NK cell receptor.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- NK cell education via nonclassical MHC and non-MHC ligands.Cellular & molecular immunology · 2017Review
- Influenza Virus Targets Class I MHC-Educated NK Cells for Immunoevasion.PLoS pathogens · 2016Article
- Natural killer cell licensing in mice with inducible expression of MHC class I.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Contrasting effects of anti-Ly49A due to MHC class I cis binding on NK cell-mediated allogeneic bone marrow cell resistance.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Targeting of a natural killer cell receptor family by a viral immunoevasin.Nature immunology · 2013Article
- Unifying concepts of MHC-dependent natural killer cell education.Trends in immunology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
NK cells become functionally competent to be triggered by their activation receptors through the interaction of NK cell inhibitory receptors with their cognate self-MHC ligands, an MHC-dependent educational process termed "licensing." For example, Ly49A(+) NK cells become licensed by the interaction of the Ly49A inhibitory receptor with its MHC class I ligand, H2D(d), whereas Ly49C(+) NK cells are licensed by H2K(b). Structural studies indicate that the Ly49A inhibitory receptor may interact with two sites, termed site 1 and site 2, on its H2D(d) ligand. Site 2 encompasses the α1/α2/α3 domains of the H2D(d) H chain and β(2)-microglobulin (β2m) and is the functional binding site for Ly49A in effector inhibition. Ly49C functionally interacts with a similar site in H2K(b). However, it is currently unknown whether this same site is involved in Ly49A- or Ly49C-dependent licensing. In this study, we produced transgenic C57BL/6 mice expressing wild-type or site 2 mutant H2D(d) molecules and studied whether Ly49A(+) NK cells are licensed. We also investigated Ly49A- and Ly49C-dependent NK licensing in murine β2m-deficient mice that are transgenic for human β2m, which has species-specific amino acid substitutions in β2m. Our data from these transgenic mice indicate that site 2 on self-MHC is critical for Ly49A- and Ly49C-dependent NK cell licensing. Thus, NK cell licensing through Ly49 involves specific interactions with its MHC ligand that are similar to those involved in effector inhibition.
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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.