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@ARTICLE{Rafei:301770,
author = {H. Rafei and R. Basar and S. Acharya and Y.-S. Hsu and P.
Liu and D. Zhang and T. Bohn$^*$ and Q. Liang and V. Mohanty
and R. Upadhyay and P. Li and P. Phadatare and M. Dede and
D. Xiong and H. Fan and C. M. Jones and S. Kunz and M. Daher
and A. K. Nunez Cortes and M. Shanley and B. Liu and S. M.
Moseley and C. Zhang and D. Fang and P. Banerjee and N.
Uprety and Y. Li and R. Shrestha and X. Wan and H. Shen and
V. Woods and A. L. Gilbert and S. Rawal and J. Dou and Y.
Tan and J.-M. Park and F. Reyes Silva and A. Biederstädt
and M. Kaplan and X. R. Jiang and I. Biederstädt and B.
Kumar and S. Tiberti and M. Moore and J. Jin and R. Z. Yang
and L. Muniz-Feliciano and S. Rosemore and P. Lin and G. M.
Deyter and N. W. Fowlkes and A. K. Jain and D. Marin and A.
Maitra and K. Chen and T. Bopp$^*$ and E. J. Shpall and K.
Rezvani},
title = {{CREM} is a regulatory checkpoint of {CAR} and {IL}-15
signalling in {NK} cells.},
journal = {Nature},
volume = {643},
number = {8073},
issn = {0028-0836},
address = {London [u.a.]},
publisher = {Nature Publ. Group},
reportid = {DKFZ-2025-01150},
pages = {1076-1086},
year = {2025},
note = {2025 Jul;643(8073):1076-1086},
abstract = {Chimeric antigen receptor (CAR) natural killer (NK) cell
immunotherapy offers a promising approach against cancer1-3.
However, the molecular mechanisms that regulate CAR-NK cell
activity remain unclear. Here we identify the transcription
factor cyclic AMP response element modulator (CREM) as a
crucial regulator of NK cell function. Transcriptomic
analysis revealed a significant induction of CREM in CAR-NK
cells during the peak of effector function after adoptive
transfer in a tumour mouse model, and this peak coincided
with signatures of both activation and dysfunction. We
demonstrate that both CAR activation and interleukin-15
signalling rapidly induce CREM upregulation in NK cells.
Functionally, CREM deletion enhances CAR-NK cell effector
function both in vitro and in vivo and increases resistance
to tumour-induced immunosuppression after rechallenge.
Mechanistically, we establish that induction of CREM is
mediated by the PKA-CREB signalling pathway, which can be
activated by immunoreceptor tyrosine-based activation motif
signalling downstream of CAR activation or by
interleukin-15. Finally, our findings reveal that CREM
exerts its regulatory functions through epigenetic
reprogramming of CAR-NK cells. Our results provide support
for CREM as a therapeutic target to enhance the antitumour
efficacy of CAR-NK cells.},
cin = {FM01},
ddc = {500},
cid = {I:(DE-He78)FM01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40468083},
doi = {10.1038/s41586-025-09087-8},
url = {https://inrepo02.dkfz.de/record/301770},
}