期刊
JOURNAL OF INTERNAL MEDICINE
卷 269, 期 1, 页码 64-73出版社
WILEY
DOI: 10.1111/j.1365-2796.2010.02317.x
关键词
cancer; dendritic cells; T cells; vaccines
资金
- NIH [P01 CA084514, U19 AIO57234, R01 CA089440, CA078846]
- Dana Foundation
- Susan Komen Foundation
- Baylor Health Care System
- Baylor Health Care System Foundation
- ANRS
- INSERM
- NATIONAL CANCER INSTITUTE [R01CA089440, R01CA140602, P01CA084512, R01CA078846] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI068842, U19AI057234] Funding Source: NIH RePORTER
T cells can reject established tumours when adoptively transferred into patients, thereby demonstrating the power of the immune system for cancer therapy. However, it has proven difficult to maintain adoptively transferred T cells in the long term. Vaccines have the potential to induce tumour-specific effector and memory T cells. However, clinical efficacy of current vaccines is limited, possibly because tumours skew the immune system by means of myeloid-derived suppressor cells, inflammatory type 2 T cells and regulatory T cells (Tregs), all of which prevent the generation of effector cells. To improve the clinical efficacy of cancer vaccines in patients with metastatic disease, we need to design novel and improved strategies that can boost adaptive immunity to cancer, help overcome Tregs and allow the breakdown of the immunosuppressive tumour microenvironment. This can be achieved by exploiting the fast increasing knowledge about the dendritic cell (DC) system, including the existence of distinct DC subsets that respond differentially to distinct activation signals, (functional plasticity), both contributing to the generation of unique adaptive immune responses. We foresee that these novel cancer vaccines will be used as monotherapy in patients with resected disease and in combination with drugs targeting regulatory/suppressor pathways in patients with metastatic disease.
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