The transcription factor EHF promotes the maturation and immunosuppression of conventional dendritic cells
The transcriptional program that regulates immunosuppression in CCR7<sup>+</sup> conventional dendritic cells (cDCs) is currently unknown. Here, we identify ETS homologous factor (EHF) as a transcription factor that regulates cDC maturation and immunosuppression after TLR7/8/9 stimulation. Mice with conditional deletion of EHF in DCs exhibit increased resistance to autoimmune, infection or tumor challenge. EHF-deficient DCs promotes Th1- and Th17-biased CD4<sup>+</sup> helper T cell response in vivo and in vitro. EHF-deficient cDC1s and cDC2s exhibit decreased expression of CCR7, CD200 and PD-L1, increased expression of DC-lineage transcriptional factor IRF4, and decreased expression of inhibitory NFκB family member Rel. EHF overexpression in DCs results in the opposite phenotype. CUT&TAG analysis suggests that EHF directly regulate Ccr7, Cd200, Cd274, Irf4 and Rel expression. Additionally, single-cell RNA-sequencing demonstrates that Ehf expression is highly enriched in CCR7<sup>hi</sup> DCs in mice and humans. Our study thus reveals a conserved transcriptional program that regulates cDC maturation and immunosuppression.
Authors
- Cliff Y. Yang (ORCID: https://orcid.org/0000-0002-2162-2912)
- Hai Ni (ORCID: https://orcid.org/0009-0004-0156-1704)
- XiaoLi Liu
- Ling Wang
- Angela R. Wu
- Jiancheng Huang
- Wei Zhao
- Jijun Zhao
- Kai Yao
- Jian-Rong Yang
- Yongfang Xiao
Institutions
- Sun Yat-sen University (CN)
- Hong Kong University of Science and Technology (HK)
- The First Affiliated Hospital, Sun Yat-sen University (CN)
- Guangdong Academy of Medical Sciences (CN)
- Guangdong Provincial People's Hospital (CN)
- Southern Medical University (CN)
- University of Hong Kong (HK)
Publication Details
- Journal
- Nature Communications
- Published
- 2026-02-23
- DOI
- https://doi.org/10.1038/s41467-026-69959-z
- Primary Topic
- Immunotherapy and Immune Responses
- Type
- article
- Field-Weighted Citation Impact
- 0.00