期刊
CELL REPORTS
卷 15, 期 5, 页码 1088-1099出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.04.005
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资金
- Swedish Research Council
- Swedish Children's Cancer Society
- Swedish Cancer Society
- Tobias Foundation
- Swedish Foundation for Strategic Research
- Karolinska Institutet
- Wenner-Gren Foundation
- Norwegian Cancer Society
- Norwegian Research Council
- South-Eastern Norway Regional Health Authority
- KG Jebsen Center for Cancer Immunotherapy
- MRC
- Welcome Trust
- National Institute for Health Research Cambridge Biomedical Research Centre
- French National Research Agency (ANR) [NKIR-ANR-13-PDOC-0025-01]
Infection by human cytomegalovirus (HCMV) leads to NKG2C-driven expansion of adaptive natural killer (NK) cells, contributing to host defense. However, approximately 4% of all humans carry a homozygous deletion of the gene that encodes NKG2C (NKG2C-/-). Assessment of NK cell repertoires in 60 NKG2C-/- donors revealed a broad range of NK cell populations displaying characteristic footprints of adaptive NK cells, including a terminally differentiated phenotype, functional reprogramming, and epigenetic remodeling of the interferon (IFN)-gamma promoter. We found that both NKG2C(-) and NKG2C(+) adaptive NK cells expressed high levels of CD2, which synergistically enhanced ERK and S6RP phosphorylation following CD16 ligation. Notably, CD2 co-stimulation was critical for the ability of adaptive NK cells to respond to antibody-coated target cells. These results reveal an unexpected redundancy in the human NK cell response to HCMV and suggest that CD2 provides signal 2'' in antibody-driven adaptive NK cell responses.
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