期刊
SCIENCE
卷 355, 期 6332, 页码 1423-1427出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaf0683
关键词
-
资金
- Merck [52507]
- National Institutes of Health [R01 AI30048, P01 AI080192, P01 AI056299, P01 AI054456, R01 AI089955, R01 CA72669, R01 AI037691]
Programmed cell death-1 (PD-1)-targeted therapies enhance T cell responses and show efficacy in multiple cancers, but the role of costimulatory molecules in this T cell rescue remains elusive. Here, we demonstrate that the CD28/B7 costimulatory pathway is essential for effective PD-1 therapy during chronic viral infection. Conditional gene deletion showed a cell-intrinsic requirement of CD28 for CD8 T cell proliferation after PD-1 blockade. B7-costimulation was also necessary for effective PD-1 therapy in tumor-bearing mice. In addition, we found that CD8 T cells proliferating in blood after PD-1 therapy of lung cancer patients were predominantly CD28-positive. Taken together, these data demonstrate CD28-costimulation requirement for CD8 T cell rescue and suggest an important role for the CD28/B7 pathway in PD-1 therapy of cancer patients.
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