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Cell Mol Immunol. 2019 Nov;16(11):868-877. doi: 10.1038/s41423-018-0169-x. Epub 2018 Oct 1.

NKR-P1B expression in gut-associated innate lymphoid cells is required for the control of gastrointestinal tract infections.

Author information

1
Department of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Road, Ottawa, ON, K1H 8M5, Canada.
2
Department of Immunology, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
3
Sunnybrook Research Institute, 2075 Bayview Avenue, Toronto, ON, M4N 3M5, Canada.
4
Department of Microbiology and Immunology, Dalhousie University, 5850 College Street, Halifax, NS, B3H 4R2, Canada.
5
College of Applied Medical Sciences, Taibah University, Madinah Munawwarah, Saudi Arabia.
6
Division of Anatomical Pathology, Department of Pathology and Laboratory Medicine, The Ottawa Hospital, University of Ottawa, 501 Smyth Road, Ottawa, ON, K1H 8L6, Canada.
7
Department of Microbiology and Immunology, Dalhousie University, 5850 College Street, Halifax, NS, B3H 4R2, Canada. munirrahimm@dal.ca.
8
Department of Microbiology and Immunology, Dalhousie University, 5850 College Street, Halifax, NS, B3H 4R2, Canada. amakrigiannis@dal.ca.

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.

KEYWORDS:

Gut-associated immune cells; Innate immunity; Innate lymphoid cells; NKR-P1B receptor; Natural killer cells

PMID:
30275537
PMCID:
PMC6828740
[Available on 2020-11-01]
DOI:
10.1038/s41423-018-0169-x

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