Tumor-derived NKG2D ligand sMIC reprograms NK cells to an inflammatory phenotype through CBM signalosome activation

Dhar et al used primary human and mouse natural killer (NK) cells to demonstrate that tumor-derived NKG2D ligand soluble MIC (sMIC) can reprogram the NK cells to secrete pro-tumorigenic cytokines with diminished cytotoxicity and polyfunctional potential. Their study provides a rationale for co-targe...

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Autores principales: Payal Dhar, Fahmin Basher, Zhe Ji, Lei Huang, Si Qin, Derek A. Wainwright, Jerid Robinson, Shaye Hagler, Jing Zhou, Sean MacKay, Jennifer D. Wu
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/0aee9ce5734644cbbebb591f8c4256a4
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spelling oai:doaj.org-article:0aee9ce5734644cbbebb591f8c4256a42021-12-02T16:26:20ZTumor-derived NKG2D ligand sMIC reprograms NK cells to an inflammatory phenotype through CBM signalosome activation10.1038/s42003-021-02440-32399-3642https://doaj.org/article/0aee9ce5734644cbbebb591f8c4256a42021-07-01T00:00:00Zhttps://doi.org/10.1038/s42003-021-02440-3https://doaj.org/toc/2399-3642Dhar et al used primary human and mouse natural killer (NK) cells to demonstrate that tumor-derived NKG2D ligand soluble MIC (sMIC) can reprogram the NK cells to secrete pro-tumorigenic cytokines with diminished cytotoxicity and polyfunctional potential. Their study provides a rationale for co-targeting sMIC in order to enhance current NK cell-based cancer immunotherapies.Payal DharFahmin BasherZhe JiLei HuangSi QinDerek A. WainwrightJerid RobinsonShaye HaglerJing ZhouSean MacKayJennifer D. WuNature PortfolioarticleBiology (General)QH301-705.5ENCommunications Biology, Vol 4, Iss 1, Pp 1-16 (2021)
institution DOAJ
collection DOAJ
language EN
topic Biology (General)
QH301-705.5
spellingShingle Biology (General)
QH301-705.5
Payal Dhar
Fahmin Basher
Zhe Ji
Lei Huang
Si Qin
Derek A. Wainwright
Jerid Robinson
Shaye Hagler
Jing Zhou
Sean MacKay
Jennifer D. Wu
Tumor-derived NKG2D ligand sMIC reprograms NK cells to an inflammatory phenotype through CBM signalosome activation
description Dhar et al used primary human and mouse natural killer (NK) cells to demonstrate that tumor-derived NKG2D ligand soluble MIC (sMIC) can reprogram the NK cells to secrete pro-tumorigenic cytokines with diminished cytotoxicity and polyfunctional potential. Their study provides a rationale for co-targeting sMIC in order to enhance current NK cell-based cancer immunotherapies.
format article
author Payal Dhar
Fahmin Basher
Zhe Ji
Lei Huang
Si Qin
Derek A. Wainwright
Jerid Robinson
Shaye Hagler
Jing Zhou
Sean MacKay
Jennifer D. Wu
author_facet Payal Dhar
Fahmin Basher
Zhe Ji
Lei Huang
Si Qin
Derek A. Wainwright
Jerid Robinson
Shaye Hagler
Jing Zhou
Sean MacKay
Jennifer D. Wu
author_sort Payal Dhar
title Tumor-derived NKG2D ligand sMIC reprograms NK cells to an inflammatory phenotype through CBM signalosome activation
title_short Tumor-derived NKG2D ligand sMIC reprograms NK cells to an inflammatory phenotype through CBM signalosome activation
title_full Tumor-derived NKG2D ligand sMIC reprograms NK cells to an inflammatory phenotype through CBM signalosome activation
title_fullStr Tumor-derived NKG2D ligand sMIC reprograms NK cells to an inflammatory phenotype through CBM signalosome activation
title_full_unstemmed Tumor-derived NKG2D ligand sMIC reprograms NK cells to an inflammatory phenotype through CBM signalosome activation
title_sort tumor-derived nkg2d ligand smic reprograms nk cells to an inflammatory phenotype through cbm signalosome activation
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/0aee9ce5734644cbbebb591f8c4256a4
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