Content area

Abstract

Background

Chimeric antigen receptor (CAR)-NK cells are a promising and safe alternative to CAR-T cells. However, the limited persistence in vivo restricts their clinical application and sustained therapeutic responses. IL-15 has been extensively used to improve CAR-NK cell persistence and effectiveness. Nevertheless, accumulation of IL-15 might induce uncontrolled proliferation of CAR-NK cells and thus lead to fatal side-effects. Therefore, it is essential to develop a safe and effective alternative strategy to improve the persistence and anti-tumor activity of CAR-NK cells.

Methods

A signaling intact membrane-bound IL-15 (mbIL-15) was designed by fusing IL-15 and full-length IL-15Rα and was systematically compared with secretory IL-15 (sIL-15) in a B7H3-targeting CAR-NK cell system regarding their functionality and safety through various in vitro and in vivo experiments.

Results

Both expression of sIL-15 or mbIL-15 significantly enhanced the proliferation by activating STAT5 and improved anti-tumor activity of CAR-NK cells in vitro and in vivo . Although CAR-NK cells with sIL-15 quickly eliminated intraperitoneal ovarian cancer, the mice experienced severe consequences, including dysregulated CAR-NK cell expansion, intense inflammatory responses, and irreversible organ damages. In contrast, CAR-NK cells carrying mbIL-15 showed moderate cell proliferation and potent tumor killing activity without observable adverse effects in both local treatment and systemic administration models.

Conclusion

Head-to-head comparative studies demonstrated that signaling intact mbIL-15 significantly improved therapeutic efficacy and safety of CAR-NK cells compared to sIL-15, which provided preclinical evidence for future clinical development.

Details

1009240
Business indexing term
Title
Signaling intact membrane-bound IL-15 enables potent anti-tumor activity and safety of CAR-NK cells
Author
Xu, Xiaodi 1 ; Cao, Peiyu 1 ; Wang, Meng 2 ; Wan, Yan 1 ; Sun, Shuwen 1 ; Chen, Yuxin 2 ; Liu, Yilin 1 ; Su, Tong 2 ; Gao, Ge 2 ; Liu, Xinze 3 ; Zhong, Weixiang 1 ; Chen, Xi 1 ; Lu, Xiaoyuan 4 ; Chen, Buze 5 ; Zheng, Junnian 6 ; Wang, Gang 2 ; Li, Huizhong 2 

 Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu, China 
 Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu, China, Center of Clinical Oncology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China, Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Xuzhou Medical University, Xuzhou, Jiangsu, China 
 The Second Clinical Medical School, Nanjing Medical University, Nanjing, Jiangsu, China 
 Department of Obstetrics and Gynecology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China 
 Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu, China, Department of Obstetrics and Gynecology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China 
 Center of Clinical Oncology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China, Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Xuzhou Medical University, Xuzhou, Jiangsu, China 
Publication title
Volume
16
First page
1658580
Number of pages
17
Publication year
2025
Publication date
Sep 2025
Section
Cancer Immunity and Immunotherapy
Publisher
Frontiers Media SA
Place of publication
Lausanne
Country of publication
Switzerland
Publication subject
e-ISSN
16643224
Source type
Scholarly Journal
Language of publication
English
Document type
Journal Article
Publication history
 
 
Online publication date
2025-09-30
Milestone dates
2025-07-02 (Recieved); 2025-09-16 (Accepted)
Publication history
 
 
   First posting date
30 Sep 2025
ProQuest document ID
3278317277
Document URL
https://www.proquest.com/scholarly-journals/signaling-intact-membrane-bound-il-15-enables/docview/3278317277/se-2?accountid=208611
Copyright
© 2025. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Last updated
2025-12-09
Database
2 databases
  • ProQuest One Academic
  • ProQuest One Academic