ArticleThe Journal of experimental medicine1997
Ly49A transgenic mice provide evidence for a major histocompatibility complex-dependent education process in natural killer cell development.
Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 97 citations in OpenAlex.
- Natural killer cells in kidney immune surveillance, injury and fibrosis.Nature reviews. Nephrology · 2026Review
- NK Cell Development in Times of Innate Lymphoid Cell Diversity.Frontiers in immunology · 2020Review
- Novel Approach to Cell Surface Discrimination Between KIR2DL1 Subtypes and KIR2DS1 Identifies Hierarchies in NK Repertoire, Education, and Tolerance.Frontiers in immunology · 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
- Newtonian cell interactions shape natural killer cell education.Immunological reviews · 2015Review
- Article
- Impaired natural killer cell self-education and "missing-self" responses in Ly49-deficient mice.Blood · 2012Article
- How the virus outsmarts the host: function and structure of cytomegalovirus MHC-I-like molecules in the evasion of natural killer cell surveillance.Journal of biomedicine & biotechnology · 2011Review
- Article
- Natural killer cell education and tolerance.Cell · 2010Review
- Probing natural killer cell education by Ly49 receptor expression analysis and computational modelling in single MHC class I mice.PloS one · 2009Article
- H-2D ligand expression by Ly49A+ natural killer (NK) cells precludes ligand uptake from environmental cells: implications for NK cell function.The Journal of experimental medicine · 2001Article
- Expression of natural killer receptor alleles at different Ly49 loci occurs independently and is regulated by major histocompatibility complex class I molecules.The Journal of experimental medicine · 2001Article
- Ly49 gene expression in different inbred mouse strains.Immunologic research · 2000Review
- Modulation of Ly49A receptors on mature cells to changes in major histocompatibility complex class I molecules.Immunology · 1998Article
- Acquisition of Ly49 receptor expression by developing natural killer cells.The Journal of experimental medicine · 1998Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Ly49 natural killer (NK) cell receptors are class I MHC-specific inhibitory receptors that are distributed to overlapping NK cell subsets. The formation of the Ly49 receptor repertoire was examined with transgenic mice that express Ly49A in all NK cells. In MHC class I-deficient mice, the Ly49A transgene did not prevent expression of endogenous Ly49 genes. However, in H-2(d) mice that express a Ly49A ligand, the transgene caused clear alterations in the endogenous Ly49 repertoire. The frequency of NK cells expressing another H-2(d)-specific receptor, Ly49G2(+), was substantially reduced. Reduced numbers of cells expressing endogenous Ly49A was suggested by reduced endogenous Ly49A mRNA levels. These results support the existence of an MHC-dependent education process that limits the number of NK cells that coexpress multiple self-specific Ly49 receptors. Ligand-dependent downregulation of Ly49 cell surface levels was also examined. Cell-surface downregulation occurred even when the transgene was expressed at low levels. The results demonstrate that downregulation of Ly49A cell surface levels is a posttranscriptional event, and argue against a model in which Ly49 receptors are calibrated to specific cell surface levels depending on the available class I ligands.
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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.