Journal
INTERNATIONAL IMMUNOLOGY
Volume 30, Issue 12, Pages 559-567Publisher
OXFORD UNIV PRESS
DOI: 10.1093/intimm/dxy050
Keywords
antibody drug; cancer immunotherapy; tumor microenvironment; TIL
Categories
Funding
- Ministry of Education, Culture, Sports, Science and Technology (MEXT Japan) [26221305, 18H02892, 15K08524, 15K06838, 18K07257, 17K15715, 18K19466]
- Uehara Memorial Foundation
- Astellas Foundation for Research on Metabolic Disorders
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [15K08524, 18K07257, 18H02892, 17K15715, 18K19466, 15K06838] Funding Source: KAKEN
Ask authors/readers for more resources
The introduction of immune checkpoint inhibitors in cancer treatment highlights the negative regulation of anti-tumor immunity, such as effector T-cell exhaustion in the tumor microenvironment. However, the mechanisms underlying the induction and prevention of T-cell exhaustion remain largely unknown. We found that CD69, a type II glycoprotein known to regulate inflammation through T-cell migration and retention in tissues, plays an important role in inducing the exhaustion of tumor-infiltrating T cells. Cd69(-/-) mice showed reduced tumor growth and metastasis in a 4T1-luc2 murine breast cancer model, in which increased numbers of tumor-infiltrating lymphocytes, relatively little T-cell exhaustion, and enhanced IFN gamma production were observed. Anti-CD69 monoclonal antibody treatment attenuated the T-cell exhaustion and tumor progression in tumor-bearing mice. These findings highlight a novel role of CD69 in controlling the tumor immune escape mediated by T-cell exhaustion and indicate that CD69 is a novel target for cancer immunotherapy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available