ArticleProceedings of the National Academy of Sciences of the United States of America1996
The natural killer cell receptor Ly-49A recognizes a peptide-induced conformational determinant on its major histocompatibility complex class I ligand.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Controlling natural killer cell responses: integration of signals for activation and inhibition.Annual review of immunology · 2013Review
- Recognition of class I MHC by a rat Ly49 NK cell receptor is dependent on the identity of the P2 anchor amino acid of bound peptide.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Distinct MHC class I-dependent NK cell-activating receptors control cytomegalovirus infection in different mouse strains.The Journal of experimental medicine · 2011Article
- Ly49-dependent NK cell licensing and effector inhibition involve the same interaction site on MHC ligands.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Efficacy and limitations of natural killer cell depletion in cyclophosphamide-induced tolerance.Surgery today · 2007Article
- Major histocompatibility complex molecules on parenchymal cells of the target organ protect against autoimmune disease.Chemical immunology and allergy · 2007Review
- The functional binding site for the C-type lectin-like natural killer cell receptor Ly49A spans three domains of its major histocompatibility complex class I ligand.The Journal of experimental medicine · 2001Article
- Activating Ly-49D and inhibitory Ly-49A natural killer cell receptors demonstrate distinct requirements for interaction with H2-D(d).The Journal of experimental medicine · 2000Article
- Article
- Structure of human histocompatibility leukocyte antigen (HLA)-Cw4, a ligand for the KIR2D natural killer cell inhibitory receptor.The Journal of experimental medicine · 1999Article
- Mouse Ly-49D recognizes H-2Dd and activates natural killer cell cytotoxicity.The Journal of experimental medicine · 1999Article
- Mouse CD94/NKG2A is a natural killer cell receptor for the nonclassical major histocompatibility complex (MHC) class I molecule Qa-1(b).The Journal of experimental medicine · 1998Article
- HLA class I specificity for natural killer cell receptor CD94/NKG2A: two for one in more ways than one.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- The mother-child union: the case of missing-self and protection of the fetus.Proceedings of the National Academy of Sciences of the United States of America · 1997Review
- Peptides isolated from HLA-Cw*0304 confer different degrees of protection from natural killer cell-mediated lysis.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Self and viral peptides can initiate lysis by autologous natural killer cells.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- The direct binding of a p58 killer cell inhibitory receptor to human histocompatibility leukocyte antigen (HLA)-Cw4 exhibits peptide selectivity.The Journal of experimental medicine · 1997Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Natural killer (NK) cells are inhibited from killing cellular targets by major histocompatibility complex (MHC) class I molecules. In the mouse, this can be mediated by the Ly-49A NK cell receptor that specifically binds the H-2Dd MHC class I molecule, then inhibits NK cell activity. Previous experiments have indicated that Ly-49A recognizes the alpha 1/alpha 2 domains of MHC class I and that no specific MHC-bound peptide appeared to be involved. We demonstrate here that alanine-substituted peptides, having only the minimal anchor motifs, stabilized H-2Dd expression and provided resistance to H-2Dd-transfected, transporter associated with processing (TAP)-deficient cells from lysis by Ly-49A+ NK cells. Peptide-induced resistance was blocked only by an mAb that binds a conformational determinant on H-2Dd. Moreover, stabilization of "empty" H-2Dd heavy chains by exogenous beta 2-microglobulin did not confer resistance. In contrast to data for MHC class I-restricted T cells that are specific for peptides displayed MHC molecules, these data indicate that NK cells are specific for a peptide-induced conformational determinant, independent of specific peptide. This fundamental distinction between NK cells and T cells further implies that NK cells are sensitive only to global changes in MHC class I conformation or expression, rather than to specific pathogen-encoded peptides. This is consistent with the "missing self" hypothesis, which postulates that NK cells survey tissues for normal expression of MHC class I.
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