The CARM1 epigenetic enzyme inhibits cross-presenting dendritic cell function in cancer immunity.

Authors

Xixi Zhang, Sherin Xirenayi, Ye Zhao, Wen Wang, Yuyang Han, Miguel Sobral, Shawn Kang, Chi Zhang, Graham L Barlow, Jason Pyrdol, Jae-Won Cho, Kun Huang, Xiaohan Ning, Martin Hemberg, Guo-Cheng Yuan, Eliezer M Van Allen, David J Mooney, Kai W Wucherpfennig

Published in

Science (New York, N.Y.). Volume 393. Issue 6807. Pages eaea1200. Jul 09, 2026. Epub Jul 09, 2026.

Abstract

The cancer-immunity cycle requires cross-presenting type I conventional dendritic cells (cDC1s) that induce T cell-mediated immunity, but therapeutic strategies for enhancing intratumoral cDC1 function are currently inadequate. We found the epigenetic enzyme CARM1 (coactivator-associated arginine methyltransferase 1) to be a selective negative regulator of cancer antigen presentation by cDC1s but not cDC2s. Inactivation of the Carm1 gene promoted cDC1 antigen cross-presentation, activation, and accumulation in tumors, and a CARM1 inhibitor enhanced cDC1-mediated priming of T cells by means of a cancer neoantigen vaccine. CARM1 inhibition increased chromatin accessibility at BATF3-Jun and RelA sites that are critical for cDC1 function and activation. Transforming growth factor-β regulated Carm1 expression, which suggests that CARM1 inactivation enhanced intratumoral cDC1 function without altering cDC1 homeostasis. These studies identify CARM1 as a potential therapeutic target for enhancing the antitumor function of mouse and human cDC1s.

PMID:
42424445
Bibliographic data and abstract were imported from PubMed on 10 Jul 2026.

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