한빛사 논문
Gi Beom Kim1,2,*, Gi-Hoon Nam1,2,*, Yeonsun Hong1,2, Jiwan Woo3, Yakdol Cho3, Ick Chan Kwon1,2, Yoosoo Yang2,4,† and In-San Kim1,2,†
1KU-KIST Graduate School of Converging Science and Technology, Korea University, 145, Anam-ro, Seongbuk-gu, Seoul 02841, Republic of Korea.
2Biomedical Research Institute, Korea Institute of Science and Technology (KIST), Seoul 02792, Republic of Korea.
3Research Animal Resource Center, Korea Institute of Science and Technology (KIST), Seoul 02792, Republic of Korea.
4Division of Bio-Medical Science & Technology, KIST School, Korea University of Science and Technology, Seoul 02792, Republic of Korea.
†Corresponding author.
*These authors contributed equally to this work.
Abstract
Many cancer patients not responding to current immunotherapies fail to produce tumor-specific T cells for various reasons, such as a lack of recognition of cancer cells as foreign. Here, we suggest a previously unidentified method for xenogenizing (turning self to non-self) tumors by using fusogenic exosomes to introduce fusogenic viral antigens (VSV-G) onto the tumor cell surface. We found that xenogenized tumor cells were readily recognized and engulfed by dendritic cells; thereby, tumor antigens were efficiently presented to T lymphocytes. Moreover, exosome–VSV-G itself acts as a TLR4 agonist and stimulates the maturation of dendritic cells, leading to CD8+ T cell cross-priming. The administration of these exosomes in multiple tumor mouse models xenogenized tumor cells, resulting in tumor growth inhibition. The combinatorial treatment with anti–PD-L1 exhibited complete tumor regression (30%) and better long-term overall survival. These results suggest that tumor xenogenization by fusogenic exosomes provides a previously unidentified novel strategy for cancer immunotherapy.
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