ArticleBlood2012
Impaired natural killer cell self-education and "missing-self" responses in Ly49-deficient mice.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 68 citations in OpenAlex.
- Ly49G, but not Ly49C/I, is dispensable for diverse antigen-specific memory NK cell responses in H-2d and H-2b mice.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- 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
- Review
- Genotype-specific expression ofbioRxiv : the preprint server for biology · 2024Article
- The inhibitory NKR-P1B receptor regulates NK cell-mediated mammary tumor immunosurveillance in mice.Oncoimmunology · 2023Article
- Natural killer cells: a promising immunotherapy for cancer.Journal of translational medicine · 2022Review
- NK cells require immune checkpoint receptor LILRB4/gp49B to control neurotropic Zika virus infections in mice.JCI insight · 2022Article
- Dynamic variability in SHP-1 abundance determines natural killer cell responsiveness.Science signaling · 2021Article
- Natural killer cells in inflammatory autoimmune diseases.Clinical & translational immunology · 2021Review
- Decreased iKIR-HLA C Pair Confers Worse Clinical Outcomes for Patients With Myeloid Disease Receiving Antithymocyte Globulin-Based Haploidentical Hematopoietic Stem Cell Transplantation.Frontiers in immunology · 2020Article
- NK Cell Priming From Endogenous Homeostatic Signals Is Modulated by CIS.Frontiers in immunology · 2020Article
- NKR-P1B expression in gut-associated innate lymphoid cells is required for the control of gastrointestinal tract infections.Cellular & molecular immunology · 2019Article
- Synergized regulation of NK cell education by NKG2A and specific Ly49 family members.Nature communications · 2019Article
- Shp-2 is critical for ERK and metabolic engagement downstream of IL-15 receptor in NK cells.Nature communications · 2019Article
- Critical role for the Ly49 family of class I MHC receptors in adaptive natural killer cell responses.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Memory responses of innate lymphocytes and parallels with T cells.Seminars in immunopathology · 2018Review
- 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
- Expression of the inhibitory receptor NKG2A correlates with increased liver and splenic NK cell response to activating receptor engagement.Immunity, inflammation and disease · 2017Article
- NK cell education via nonclassical MHC and non-MHC ligands.Cellular & molecular immunology · 2017Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
Ly49-mediated recognition of MHC-I molecules on host cells is considered vital for natural killer (NK)-cell regulation and education; however, gene-deficient animal models are lacking because of the difficulty in deleting this large multigene family. Here, we describe NK gene complex knockdown (NKC(KD)) mice that lack expression of Ly49 and related MHC-I receptors on most NK cells. NKC(KD) NK cells exhibit defective killing of MHC-I-deficient, but otherwise normal, target cells, resulting in defective rejection by NKC(KD) mice of transplants from various types of MHC-I-deficient mice. Self-MHC-I immunosurveillance by NK cells in NKC(KD) mice can be rescued by self-MHC-I-specific Ly49 transgenes. Although NKC(KD) mice display defective recognition of MHC-I-deficient tumor cells, resulting in decreased in vivo tumor cell clearance, NKG2D- or antibody-dependent cell-mediated cytotoxicity-induced tumor cell cytotoxicity and cytokine production induced by activation receptors was efficient in Ly49-deficient NK cells, suggesting MHC-I education of NK cells is a single facet regulating their total potential. These results provide direct genetic evidence that Ly49 expression is necessary for NK-cell education to self-MHC-I molecules and that the absence of these receptors leads to loss of MHC-I-dependent "missing-self" immunosurveillance by NK cells.
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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.