ArticleProceedings of the National Academy of Sciences of the United States of America2007
Stable masking by H-2Dd cis ligand limits Ly49A relocalization to the site of NK cell/target cell contact.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- Recognition of Self and Viral Ligands by NK Cell Receptors.Immunological reviews · 2025Review
- Novel Functions of Integrins as Receptors of CD154: Their Role in Inflammation and Apoptosis.Cells · 2022Review
- Homotypic and heterotypicCurrent research in immunology · 2022Review
- Licensing Natural Killers for Antiviral Immunity.Pathogens (Basel, Switzerland) · 2021Review
- Article
- The complex of MCMV proteins and MHC class I evades NK cell control and drives the evolution of virus-specific activating Ly49 receptors.The Journal of experimental medicine · 2019Article
- Novel Approach to Cell Surface Discrimination Between KIR2DL1 Subtypes and KIR2DS1 Identifies Hierarchies in NK Repertoire, Education, and Tolerance.Frontiers in immunology · 2019Article
- Inhibitory Receptor Crosslinking Quantitatively Dampens Calcium Flux Induced by Activating Receptor Triggering in NK Cells.Frontiers in immunology · 2018Article
- NK cell education via nonclassical MHC and non-MHC ligands.Cellular & molecular immunology · 2017Review
- Modulation of natural killer cell functions by interactions between 2B4 and CD48 in cis and in trans.Open biology · 2016Article
- 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
- Ly49C-dependent control of MCMV Infection by NK cells is cis-regulated by MHC Class I molecules.PLoS pathogens · 2014Article
- Structural basis for recognition of cellular and viral ligands by NK cell receptors.Frontiers in immunology · 2014Review
- 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
- Natural killer cell inhibitory receptor expression in humans and mice: a closer look.Frontiers in immunology · 2013Article
- Cis-trans interactions of cell surface receptors: biological roles and structural basis.Cellular and molecular life sciences : CMLS · 2011Review
- A modified FCCS procedure applied to Ly49A-MHC class I cis-interaction studies in cell membranes.Biophysical journal · 2011Article
- The interaction with H-2D(d) in cis is associated with a conformational change in the Ly49A NK cell receptor.Frontiers in immunology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ly49A is an inhibitory receptor, which counteracts natural killer (NK) cell activation on the engagement with H-2D(d) (D(d)) MHC class I molecules (MHC-I) on target cells. In addition to binding D(d) on apposed membranes, Ly49A interacts with D(d) ligand expressed in the plane of the NK cells' membrane. Indeed, multivalent, soluble MHC-I ligand binds inefficiently to Ly49A unless the NK cells' D(d) complexes are destroyed. However, it is not known whether masked Ly49A remains constitutively associated with cis D(d) also during target cell interaction. Alternatively, it is possible that Ly49A has to be unmasked to significantly interact with its ligand on target cells. These two scenarios suggest distinct roles of Ly49A/D(d) cis interaction for NK cell function. Here, we show that Ly49A contributes to target cell adhesion and efficiently accumulates at synapses with D(d)-expressing target cells when NK cells themselves lack D(d). When NK cells express D(d), Ly49A no longer contributes to adhesion, and ligand-driven recruitment to the cellular contact site is strongly reduced. The destruction of D(d) complexes on NK cells, which unmasks Ly49A, is necessary and sufficient to restore Ly49A adhesive function and recruitment to the synapse. Thus, cis D(d) continuously sequesters a considerable fraction of Ly49A receptors, preventing efficient Ly49A recruitment to the synapse with D(d)+ target cells. The reduced number of Ly49A receptors that can functionally interact with D(d) on target cells explains the modest inhibitory capacity of Ly49A in D(d) NK cells. This property renders Ly49A NK cells more sensitive to react to diseased host cells.
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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.