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Wando Mount Pleasant Library
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Deletion of the mRNA endonuclease Regnase-1 promotes NK cell anti-tumor activity via OCT2-dependent transcription of Ifng.
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- Author(s): Sun, Xin1,2,3 (AUTHOR); Nagahama, Yasuharu1,3,4 (AUTHOR); Singh, Shailendra Kumar1,3 (AUTHOR); Kozakai, Yuuki1 (AUTHOR); Nabeshima, Hiroshi1,3,4 (AUTHOR); Fukushima, Kiyoharu1,3,5,6 (AUTHOR); Tanaka, Hiroki1 (AUTHOR); Motooka, Daisuke7 (AUTHOR); Fukui, Eriko8 (AUTHOR); Vivier, Eric9,10,11 (AUTHOR); Diez, Diego1,2 (AUTHOR); Akira, Shizuo1,3,5,12 (AUTHOR)
- Source:
Immunity (10747613). Jun2024, Vol. 57 Issue 6, p1360-1360. 1p.- Subject Terms:
- Source:
- Additional Information
- Abstract: Limited infiltration and activity of natural killer (NK) and T cells within the tumor microenvironment (TME) correlate with poor immunotherapy responses. Here, we examined the role of the endonuclease Regnase-1 on NK cell anti-tumor activity. NK cell-specific deletion of Regnase-1 (Reg1 ΔNK) augmented cytolytic activity and interferon-gamma (IFN-γ) production in vitro and increased intra-tumoral accumulation of Reg1 ΔNK-NK cells in vivo , reducing tumor growth dependent on IFN-γ. Transcriptional changes in Reg1 ΔNK-NK cells included elevated IFN-γ expression, cytolytic effectors, and the chemokine receptor CXCR6. IFN-γ induced expression of the CXCR6 ligand CXCL16 on myeloid cells, promoting further recruitment of Reg1 ΔNK-NK cells. Mechanistically, Regnase-1 deletion increased its targets, the transcriptional regulators OCT2 and IκBζ, following interleukin (IL)-12 and IL-18 stimulation, and the resulting OCT2-IκBζ-NF-κB complex induced Ifng transcription. Silencing Regnase-1 in human NK cells increased the expression of IFNG and POU2F2. Our findings highlight NK cell dysfunction in the TME and propose that targeting Regnase-1 could augment active NK cell persistence for cancer immunotherapy. [Display omitted] • Regnase-1 deficiency strengthens IFN-γ-mediated anti-tumor immunity of NK cells • IFN-γ-induced CXCL16 detains CXCR6+ mature NK cells in tumor microenvironment • Regnase-1-null NK cells induce a widespread increase in chromatin accessibility • The complex of OCT2, IκBζ, and NF-κB collaborates in the transcription of Ifng Low persistence and reduced activity of NK cells limit anti-tumor immunity. Sun, Nagahama, et al. find that NK cell-specific deficiency of the endonuclease Regnase-1 promotes NK cell persistence in the tumor microenvironment via continuous expression of CXCR6 and enhances anti-tumor activity through increased Ifng transcription mediated by OCT2. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Immunity (10747613) is the property of Cell Press and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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