ArticleThe Journal of experimental medicine1995
NKR-P1A is a target-specific receptor that activates natural killer cell cytotoxicity.
Article in The Journal of experimental medicine, 1995. 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, 125 citations in OpenAlex.
- NKR-P1A/CD161: A Multifunctional Immune Receptor at the Crossroads of Antitumor Immunity.Biomolecules · 2026Review
- Reed-Sternberg cells express CD161 and lectin-like transcript 1 in Hodgkin lymphoma.Frontiers in medicine · 2026Article
- Prenatal alcohol exposure is a risk factor for adult neuropathic pain via aberrant neuroimmune function.Journal of neuroinflammation · 2017Article
- Frequency of CD4+CD161+ T Cell and Interleukin-10 Expression in Inflammatory Bowel Diseases.Acta histochemica et cytochemica · 2017Article
- Regulation of Murine Ovarian Epithelial Carcinoma by Vaccination against the Cytoplasmic Domain of Anti-Müllerian Hormone Receptor II.Journal of immunology research · 2015Article
- Complexity and Diversity of the NKR-P1:Clr (Klrb1:Clec2) Recognition Systems.Frontiers in immunology · 2014Review
- Analysis of the mouse 129-strain Nkrp1-Clr gene cluster reveals conservation of genomic organization and functional receptor-ligand interactions despite significant allelic polymorphism.Immunogenetics · 2011Article
- Chemotherapy-induced genotoxic stress promotes sensitivity to natural killer cell cytotoxicity by enabling missing-self recognition.Cancer research · 2010Article
- Article
- CD161B:ClrB interactions mediate activation of enhanced lysis of tumor target cells following NK cell:DC co-culture.Immunologic research · 2006Article
- NKR-P1 biology: from prototype to missing self.Immunologic research · 2006Review
- Missing self-recognition of Ocil/Clr-b by inhibitory NKR-P1 natural killer cell receptors.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Turning on natural killer cells.The Journal of experimental medicine · 2000Review
- Inhibitory receptors alter natural killer cell interactions with target cells yet allow simultaneous killing of susceptible targets.The Journal of experimental medicine · 1999Article
- Ly49A inhibitory receptors redistribute on natural killer cells during target cell interaction.Immunology · 1999Article
- Genetic control of natural killing and in vivo tumor elimination by the Chok locus.The Journal of experimental medicine · 1998Article
- Interferon gamma derived from CD4(+) T cells is sufficient to mediate T helper cell type 1 development.The Journal of experimental medicine · 1998Article
- CD161 (NKR-P1A) costimulation of CD1d-dependent activation of human T cells expressing invariant V alpha 24 J alpha Q T cell receptor alpha chains.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
- Functional role for Syk tyrosine kinase in natural killer cell-mediated natural cytotoxicity.The Journal of experimental medicine · 1997Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
NKR-P1A is a lectinlike surface molecule expressed on rat natural killer (NK) cells. NKR-P1A has structural and functional features of an activating NK cell receptor, but a requirement for NKR-P1A in target cell lysis has not been determined. To define the role of NKR-P1A in natural killing, we have generated a mutant of the rat NK cell line, RNK-16, lacking expression of all members of the NKR-P1 receptor family. Although these NKR-P1-deficient NK cells were able to kill many standard tumor targets, including YAC-1, they were selectively deficient in the lysis of IC-21 macrophage, B-16 melanoma, and C1498 lymphoma targets. Reexpression of a single member of the NKR-P1 family, NKR-P1A, on mutant cells restored lysis of IC-21, and killing of IC-21 targets through rat NKR-P1A was completely blocked by F(ab')2 anti-NKR-P1A. Reexpression of NKR-P1A also restored transmembrane signaling to IC-21, as assessed by the generation of inositol-1,4,5-trisphosphate. The generation of inositol-1,4,5-trisphosphate was also restored in response to B-16 targets, but both B-16 and C1498 cells remained resistant to lysis, indicating that other NK cell molecules, perhaps within the NKR-P1 family, are required for the efficient killing of these tumors. These results are the first to demonstrate that NKR-P1A is a target-specific receptor that activates natural killing.
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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.