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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Sumario: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.