EDF1 accelerates ganglioside GD3 accumulation to boost CD52-mediated CD8+ T cell dysfunction in neuroblastoma
These findings characterize abundant GD3 in NB cells, which regulated by the EDF1/RelA/ST8SIA1 axis, is responsible for CD8<sup>+</sup> T cell dysfunction. Inhibition of EDF1 may reduce suppressive factors and prevent immune escape of NB cells. Modulating NB-associated GD3 levels through metabolic intervention is beneficial for tuning the depth and duration of responses to current NB therapies. The integration of transcriptomic and lipidomic data offers a more comprehensive understanding of the interaction between LacCer metabolites and the immune status in NB.
Authors
- Jue Tang (ORCID: https://orcid.org/0000-0002-3765-277X)
- Huimin Xia (ORCID: https://orcid.org/0000-0002-0103-1672)
- Huiran Lin
- Jing He (ORCID: https://orcid.org/0000-0002-1954-2892)
- Yile Xu
- Zhenjian Zhuo (ORCID: https://orcid.org/0000-0003-0142-4086)
- Di Li (ORCID: https://orcid.org/0000-0001-6783-4542)
- Meng Li (ORCID: https://orcid.org/0000-0002-8000-3003)
- Haiyun Wang (ORCID: https://orcid.org/0000-0002-1385-0827)
- Lei Miao (ORCID: https://orcid.org/0000-0001-7670-4782)
- Weixin Zhang (ORCID: https://orcid.org/0000-0002-1009-101X)
- Huiqin Guo
- Jiabin Liu
Institutions
- Chinese Academy of Sciences (CN)
- Peking University (CN)
- Guangzhou Women and Children Medical Center (CN)
- Shenzhen Institutes of Advanced Technology (CN)
- Guangzhou Medical University (CN)
Publication Details
- Journal
- Journal of Experimental & Clinical Cancer Research
- Published
- 2025-02-04
- DOI
- https://doi.org/10.1186/s13046-025-03307-9
- Citations
- 3
- Primary Topic
- Neuroblastoma Research and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 4.17
Funders
- National Natural Science Foundation of China