Disrupting Notch signaling related HES1 in myeloid cells reinvigorates antitumor T cell responses
We identified a pivotal role for the Notch signaling pathway in shaping TAM function, suggesting that T-cell dysfunction in the TME is caused when the Notch target, HES1, in TAMs is upregulated by tumor-associated factors (TAFs), which, in turn, increases the expression of arginase-1. Targeting HES1 in TAMs appears to be a promising strategy for cancer immunotherapy.
Authors
- Hyeok-Gu Kang (ORCID: https://orcid.org/0000-0002-3187-6844)
- Kyung‐Hee Chun (ORCID: https://orcid.org/0000-0002-9867-7321)
- Eun Joo Chung (ORCID: https://orcid.org/0000-0001-8948-1135)
- Joon‐Yong Chung (ORCID: https://orcid.org/0000-0001-5041-5982)
- Moon-Gyu Cho
- Seok‐Jun Kim (ORCID: https://orcid.org/0000-0002-7498-1775)
- Jung-Hwan Baek
- Myung Sup Kim
Institutions
- Pohang University of Science and Technology (KR)
- National Institutes of Health (US)
- Chosun University (KR)
- Yonsei University (KR)
- National Cancer Institute (US)
- Center for Cancer Research (US)
- Yonsei University Health System (KR)
Publication Details
- Journal
- Experimental Hematology and Oncology
- Published
- 2024-12-19
- DOI
- https://doi.org/10.1186/s40164-024-00588-2
- Citations
- 8
- Primary Topic
- Immune cells in cancer
- Type
- article
- Field-Weighted Citation Impact
- 1.92
Funders
- National Research Foundation
- Yonsei University
- National Research Foundation of Korea
- Ministry of Science and ICT, South Korea
- Yonsei University College of Medicine