Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 120, Issue 1, Pages 76-80Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI41811
Keywords
-
Categories
Funding
- NATIONAL CANCER INSTITUTE [R01CA105216] Funding Source: NIH RePORTER
- NCI NIH HHS [5R01CA105216, R01 CA105216-05, R01 CA105216] Funding Source: Medline
Ask authors/readers for more resources
Attenuating coinhibitory molecules for the treatment of cancer is gaining a great deal of attention as a strategy for immunotherapy. The B and T lymphocyte attenuator (BTLA, CD272) is a novel coinhibitory molecule structurally and functionally related to CTLA-4 and PD-1. A study in this issue of the JCI by Derre et at. reveals that BTLA is expressed on virus-specific human CD8(+) T cells but is progressively downregulated after their differentiation from a naive to effector phenotype (see the related article beginning on page 157). Surprisingly, tumor-specific human CD8(+) T cells continue to express BTLA even after their differentiation to an effector phenotype. Remarkably, vaccination of melanoma patients with CpG led to BTLA downregulation on tumor-specific human CD8(+) T cells, concomitant with restoration of their functionality. We discuss these findings in the context of the expanding field of cosignaling molecules and their implications for T cell-based therapies for cancer.
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