ArticleCellular & molecular immunology2019
NKR-P1B expression in gut-associated innate lymphoid cells is required for the control of gastrointestinal tract infections.
Article in Cellular & molecular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Effects of Habitual Dietary Change on the Gut Microbiota and Health of Silkworms.International journal of molecular sciences · 2024Article
- The diverse roles of C-type lectin-like receptors in immunity.Frontiers in immunology · 2023Review
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- Alveolar macrophage metabolic programming via a C-type lectin receptor protects against lipo-toxicity and cell death.Nature communications · 2022Article
- Clr-f expression regulates kidney immune and metabolic homeostasis.Scientific reports · 2022Article
- Innate lymphoid cells and cancer: Role in tumor progression and inhibition.European journal of immunology · 2021Review
- Type 3 Innate Lymphoid Cells as Regulators of the Host-Pathogen Interaction.Frontiers in immunology · 2021Review
- Innate Lymphoid Cells: Important Regulators of Host-Bacteria Interaction for Border Defense.Microorganisms · 2020Review
- Natural Killer Cells: Tumor Surveillance and Signaling.Cancers · 2020Review
- The pathogenic role of innate lymphoid cells in autoimmune-related and inflammatory skin diseases.Cellular & molecular immunology · 2020Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
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Abstract
Helper-type innate lymphoid cells (ILC) play an important role in intestinal homeostasis. Members of the NKR-P1 gene family are expressed in various innate immune cells, including natural killer (NK) cells, and their cognate Clr ligand family members are expressed in various specialized tissues, including the intestinal epithelium, where they may play an important role in mucosal-associated innate immune responses. In this study, we show that the inhibitory NKR-P1B receptor, but not the Ly49 receptor, is expressed in gut-resident NK cells, ILC, and a subset of γδT cells in a tissue-specific manner. ILC3 cells constitute the predominant cell subset expressing NKR-P1B in the gut lamina propria. The known NKR-P1B ligand Clr-b is broadly expressed in gut-associated cells of hematopoietic origin. The genetic deletion of NKR-P1B results in a higher frequency and number of ILC3 and γδT cells in the gut lamina propria. However, the function of gut-resident ILC3, NK, and γδT cells in NKR-P1B-deficient mice is impaired during gastrointestinal tract infection by Citrobacter rodentium or Salmonella typhimurium, resulting in increased systemic bacterial dissemination in NKR-P1B-deficient mice. Our findings highlight the role of the NKR-P1B:Clr-b recognition system in the modulation of intestinal innate immune cell functions.
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