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About the Authors:
Yufeng Wang
Contributed equally to this work with: Yufeng Wang, Wenjuan Dong, Yibo Zhang
Roles Formal analysis, Investigation, Methodology, Writing - original draft
Affiliation: The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, United States of America
Wenjuan Dong
Contributed equally to this work with: Yufeng Wang, Wenjuan Dong, Yibo Zhang
Roles Formal analysis, Investigation, Methodology
Affiliation: The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, United States of America
Yibo Zhang
Contributed equally to this work with: Yufeng Wang, Wenjuan Dong, Yibo Zhang
Roles Formal analysis, Investigation, Methodology
Affiliation: The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, United States of America
Michael A. Caligiuri
Roles Funding acquisition, Resources
Affiliations The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, United States of America, The James Cancer Hospital, Columbus, Ohio, United States of America, Division of Hematology, Department of Medicine, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America
Jianhua Yu
Roles Conceptualization, Funding acquisition, Resources, Supervision, Writing - review & editing
* E-mail: [email protected]
Affiliations The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, United States of America, The James Cancer Hospital, Columbus, Ohio, United States of America, Division of Hematology, Department of Medicine, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America
ORCID http://orcid.org/0000-0002-0326-3223Abstract
NKp46, a natural killer (NK) cell-activating receptor, is involved in NK cell cytotoxicity against virus-infected cells or tumor cells. However, the role of NKp46 in other NKp46+ non-NK innate lymphoid cell (ILC) populations has not yet been characterized. Here, an NKp46 deficiency model of natural cytotoxicity receptor 1 (Ncr1)gfp/gfp and Ncr1gfp/+ mice, i.e., homozygous and heterozygous knockout (KO), was used to explore the role of NKp46 in regulating the development of the NKp46+ ILCs. Surprisingly, our studies demonstrated that homozygous NKp46 deficiency resulted in a nearly complete depletion of the ILC1 subset (ILC1) of group 1 ILCs, and heterozygote KO decreased the number of cells in the ILC1 subset. Moreover, transplantation studies confirmed that ILC1 development depends on NKp46 and that the dependency is cell intrinsic. Interestingly, however, the cell depletion specifically occurred in the ILC1 subset but not in the other ILCs, including ILC2s, ILC3s, and NK cells. Thus, our studies reveal that NKp46 selectively participates in...