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

X Xixi Zhang (Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.) S Sherin Xirenayi (Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.) Y Ye Zhao (Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.) W Wen Wang Y Yuyang Han (Gene Lay Institute of Immunology and Inflammation, Brigham and Women’s Hospital, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.) M Miguel Sobral (Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, USA.) S Shawn Kang (Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, USA.) C Chi Zhang G Graham L. Barlow (Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.) J Jason Pyrdol (Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.) J Jae-Won Cho (Gene Lay Institute of Immunology and Inflammation, Brigham and Women’s Hospital, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.) K Kun Huang (Molecular Imaging Core, Dana-Farber Cancer Institute, Boston, MA, USA.) X Xiaohan Ning (Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.) M Martin Hemberg (Broad Institute of Harvard and MIT, Cambridge, MA, USA.) G Guo-Cheng Yuan (Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.) E Eliezer M. Van Allen D David J. Mooney (Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, USA.) K Kai W. Wucherpfennig (Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.)

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.

Article Details

Journal Science
Volume / Issue Vol. 393, Issue 6807
Published July 09, 2026
ISSN 0036-8075
Publisher American Association for the Advancement of Science

Journal Info

Science

American Association for the Advancement of Science

ISSN: 0036-8075 Social Sciences

Authors (18)

X

Xixi Zhang

Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.

S

Sherin Xirenayi

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.

Y

Ye Zhao

Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.

W

Wen Wang

Y

Yuyang Han

Gene Lay Institute of Immunology and Inflammation, Brigham and Women’s Hospital, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

M

Miguel Sobral

Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, USA.

S

Shawn Kang

Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, USA.

C

Chi Zhang

G

Graham L. Barlow

Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.

J

Jason Pyrdol

Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.

J

Jae-Won Cho

Gene Lay Institute of Immunology and Inflammation, Brigham and Women’s Hospital, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

K

Kun Huang

Molecular Imaging Core, Dana-Farber Cancer Institute, Boston, MA, USA.

X

Xiaohan Ning

Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.

M

Martin Hemberg

Broad Institute of Harvard and MIT, Cambridge, MA, USA.

G

Guo-Cheng Yuan

Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

E

Eliezer M. Van Allen

D

David J. Mooney

Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, USA.

K

Kai W. Wucherpfennig

Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.