ArticlePloS one2016
Activation by SLAM Family Receptors Contributes to NK Cell Mediated "Missing-Self" Recognition.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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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.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Dual Regulatory Functions and Therapeutic Potential of CD48 in Tumor Immunity.Oncology research · 2026Review
- Systematic Multiomic Analysis ofInternational journal of molecular sciences · 2023Article
- Microglia and microbiome in schizophrenia: can immunomodulation improve symptoms?Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- CD229 interacts with RASAL3 to activate RAS/ERK pathway in multiple myeloma proliferation.Aging · 2022Article
- Advances in Understanding the Roles of CD244 (SLAMF4) in Immune Regulation and Associated Diseases.Frontiers in immunology · 2021Review
- Natural Killer Cells in the Malignant Niche of Multiple Myeloma.Frontiers in immunology · 2021Review
- Sperm Protein 17 Expression by Murine Epithelial Ovarian Cancer Cells and Its Impact on Tumor Progression.Cancers · 2018Article
- Granule-Dependent Natural Killer Cell Cytotoxicity to Fungal Pathogens.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Natural Killer (NK) cells attack normal hematopoietic cells that do not express inhibitory MHC class I (MHC-I) molecules, but the ligands that activate NK cells remain incompletely defined. Here we show that the expression of the Signaling Lymphocyte Activation Molecule (SLAM) family members CD48 and Ly9 (CD229) by MHC-I-deficient tumor cells significantly contributes to NK cell activation. When NK cells develop in the presence of T cells or B cells that lack inhibitory MHC-I but express activating CD48 and Ly9 ligands, the NK cells' ability to respond to MHC-I-deficient tumor cells is severely compromised. In this situation, NK cells express normal levels of the corresponding activation receptors 2B4 (CD244) and Ly9 but these receptors are non-functional. This provides a partial explanation for the tolerance of NK cells to MHC-I-deficient cells in vivo. Activating signaling via 2B4 is restored when MHC-I-deficient T cells are removed, indicating that interactions with MHC-I-deficient T cells dominantly, but not permanently, impair the function of the 2B4 NK cell activation receptor. These data identify an important role of SLAM family receptors for NK cell mediated "missing-self" reactivity and suggest that NK cell tolerance in MHC-I mosaic mice is in part explained by an acquired dysfunction of SLAM family receptors.
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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.