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NKR-p1B expression in gut-associated innate lymphoid cells is required for the control of gastrointestinal tract infections

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Cellular & Molecular Immunology 2019年第11期16卷 868-877页

作者： Elias Abou-Samra Zachary Hickey Oscar A.Aguilar Michal Scur Ahmad Bakur Mahmoud Sergey pyatibrat Megan M.Tu Jeffrey Francispillai Arthur Mortha James R.Carlyle Mir Munir A.Rahim andrew p.makrigiannis Department of Biochemistry Microbiology and ImmunologyUniversity of Ottawa451 Smyth RoadOttawaON K1H 8M5Canada Department of Immunology University of Toronto1 King’s College CircleTorontoON M5S 1A8Canada Sunnybrook Research Institute 2075 Bayview AvenueTorontoON M4N 3M5Canada Department of Microbiology and Immunology Dalhousie University5850 College StreetHalifaxNS B3H 4R2Canada College of Applied Medical Sciences Taibah UniversityMadinah MunawwarahSaudi Arabia Division of Anatomical pathology Department of Pathology and Laboratory MedicineThe Ottawa HospitalUniversity of Ottawa501 Smyth RoadOttawaON K1H 8L6Canada

Helper-type innate lymphoid cells(ILC)play an important role in intestinal *** 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 mucosalassociated innate immune *** 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 ofγδT cells in a tissue-specific ***3 cells constitute the predominant cell subset expressing NKR-p1B in the gut lamina *** known NKR-p1B ligand Clr-b is broadly expressed in gut-associated cells of hematopoietic *** genetic deletion of NKR-p1B results in a higher frequency and number of ILC3 andγδT cells in the gut lamina ***,the function of gut-resident ILC3,NK,andγδT 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 *** findings highlight the role of the NKR-p1B:Clr-b recognition system in the modulation of intestinal innate immune cell functions.

关键词： Innate lymphoid cells Natural killer cells Gut-associated immune cells NKR-p1B receptor Innate immunity

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Ly49 receptors activate angiogenic mouse DBA＋ uterine natural killer cells

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Cellular & Molecular Immunology 2014年第5期11卷 467-476页

作者： patricia DA Lima Megan M Tu Mir Munir A Rahim Annie R peng B Anne Croy andrew p.makrigiannis Department of Biochemistry Microbiologyand Immunology University of Ottawa Ottawa ON KIN 6N5 Canada Biomedical and Molecular Sciences Queen's University Kingston ON K7L 3N6 Canada

In humans, specific patterns of killer immunoglobulin-like receptors （KIRs） expressed by uterine natural killer （uNK） cells are linked through HLA-C with pregnancy complications （infertility, recurrent spontaneous abortion, intrauterine growth restriction and preeclampsia）. To identify mechanisms underpinning the associations between NK cell activation and pregnancy success, pregnancies were studied in mice with genetic knockdown （KD） of the MHC-activated Ly49 receptor gene family. ***49KD pregnancies were compared to normal control ***49z29 and C57BL/6 （B6） pregnancies. At mid-pregnancy （gestation day （gd9.5））, overall uNK cell （TCRI^-CD122＋DBA＋DX5- （DBA＋DX5-）） and TCRIβ-CD122＋DBA-DX5＋（DBA-DX5＋）） frequencies in pregnant uterus were similar between genotypes. Ly49KD lowered the normal frequencies of Ly49＋ uNK cells from 90.3% to 47.8% in DBA-DX5＋ and 78.8% to 6.3% in DBA＋DX5- uNK cell subtypes. ***49KD matings frequently resulted in expanded blastocysts that did not implant （subfertility）. ***49KD mice that established pregnancy had gestational lengths and litter sizes similar to controls. ***49KD neonates, however, were heavier than controls. ***49KD implantation sites lagged in early （gd6.5） decidual angiogenesis and were deficient in mid-pregnancy （gd 10.5） spiral arterial remodelling. Ultrastructural analyses revealed that ***49KD uNK cells had impaired granulogenesis, while immunocytochemistry revealed deficient vascular endothelial cell growth factor （VEGFA） production. perforin and IFNG expression were normal in ***49KD uNK cells. Thus, in normal mouse pregnancies, Ly49 receptor signaling must promote implantation, early decidual angiogenesis and mid-pregnancy vascular remodelling. Disturbances in these functions may underlie the reported genetic associations between human pregnancy complications and the inability of specific conceptus MHCs to engage activating KIR on uNK cells.

关键词： fetal growth deviation granule biogenesis MHC-I receptors uterine natural killer cells vascular endothelialcell growth factor

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