ArticleThe Journal of experimental medicine2001
H-2D ligand expression by Ly49A+ natural killer (NK) cells precludes ligand uptake from environmental cells: implications for NK cell function.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- NK cells in peripheral blood carry trogocytosed tumor antigens from solid cancer cells.Frontiers in immunology · 2023Article
- Trogocytosis in innate immunity to cancer is an intimate relationship with unexpected outcomes.iScience · 2022Article
- When killers become thieves: Trogocytosed PD-1 inhibits NK cells in cancer.Science advances · 2022Article
- Imprint of Initial Education and Loss of Ly49C/I in Activated Natural Killer Cells of TAP1-KO and C57BL/6 Wildtype Mice.Frontiers in immunology · 2022Article
- Review
- NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions.Nature communications · 2016Article
- Adaptations of Natural Killer Cells to Self-MHC Class I.Frontiers in immunology · 2014Article
- Antigen Presentation by MHC-Dressed Cells.Frontiers in immunology · 2014Review
- 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
- A modified FCCS procedure applied to Ly49A-MHC class I cis-interaction studies in cell membranes.Biophysical journal · 2011Article
- Unifying concepts of MHC-dependent natural killer cell education.Trends in immunology · 2011Review
- Mechanisms of cellular communication through intercellular protein transfer.Journal of cellular and molecular medicine · 2011Review
- The interaction with H-2D(d) in cis is associated with a conformational change in the Ly49A NK cell receptor.Frontiers in immunology · 2011Article
- Natural killer cell tolerance persists despite significant reduction of self MHC class I on normal target cells in mice.PloS one · 2010Article
- Current perspectives of natural killer cell education by MHC class I molecules.Nature reviews. Immunology · 2010Review
- MHC class I-deficient natural killer cells acquire a licensed phenotype after transfer into an MHC class I-sufficient environment.The Journal of experimental medicine · 2010Article
- Glycosylation contributes to variability in expression of murine cytomegalovirus m157 and enhances stability of interaction with the NK-cell receptor Ly49H.European journal of immunology · 2010Article
- Adaptive immune responses mediated by natural killer cells.Immunological reviews · 2010Review
- Effects of MHC class I alleles on licensing of Ly49A+ NK cells.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Cis interactions of immunoreceptors with MHC and non-MHC ligands.Nature reviews. Immunology · 2008Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To study the adaptation of natural killer (NK) cells to their major histocompatibility complex (MHC) class I environment we have established a novel mouse model with mosaic expression of H-2D(d) using a Cre/loxP system. In these mice, we noticed that NK cells expressing the inhibitory receptor for D(d), Ly49A, were specifically underrepresented among cells with low D(d) levels. That was due to the acquisition of D(d) molecules by the Ly49A+ NK cells that have lost their D(d) transgene. The uptake of H-2D molecules via the Ly49A receptor was restricted to strong ligands of Ly49A. Surprisingly, when Ly49A+ NK cells were D(d+), uptake of the alternative ligand D(k) was not detectable. Similarly, one anti-Ly49A mAb (A1) bound inefficiently when Ly49A was expressed on D(d+) NK cells. Concomitantly, functional assays demonstrated a reduced capacity of Ly49A to inhibit H-2(b)D(d) as compared with H-2(b) NK cells, rendering Ly49A+ NK cells in D(d+) mice particularly reactive. Minor reductions of D(d) levels and/or increases of activating ligands on environmental cells may thus suffice to abrogate Ly49A-mediated NK cell inhibition. The mechanistic explanation for all these phenomena is likely the partial masking of Ly49A by D(d) on the same cell via a lateral binding site in the H-2D(d) molecule.
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