期刊
CELLULAR IMMUNOLOGY
卷 263, 期 1, 页码 79-87出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2010.03.001
关键词
Paclitaxel; Cyclophosphamide; Dendritic cell; Cross-presentation; Immunotherapy; Immunomodulation; Combination therapy
资金
- National Cancer Institute [P50CA62924, P50CA088843]
- National Cancer Institute NCDDG [U19CA113341]
- National Cancer Institute RO1 [CA122081]
- Skip Viragh Pancreatic Center for Clinical Research and Patient Care
- Goldman Pancreatic Cancer Center
- Dana and Albert Broccoli Foundation
- NATIONAL CANCER INSTITUTE [P50CA088843, U19CA113341, P50CA062924, R01CA122081] Funding Source: NIH RePORTER
Subclinical closes of Paclitaxel (PTX) given 1 day prior to a HER-2/neu (neu)-targeted, granulocyte-macrophage colony stimulating factor (GM-CSF)-secreting whole-cell vaccine enhances neu-specific T cell responses and slows neu(+) tumor growth in tolerized HER-2/neu (neu-N) mice. We demonstrate that co-administration of PTX and Cyclophosphamide (CV) synergizes to slow tumor growth, and that in vitro. DC precursors exposed to PTX before LPS maturation results in greater co-stimulatory molecule expression, IL-12 production, and the ability to induce CD8(+) T cells with enhanced lytic activity against neu(+) tumors. PTX treatment also enhances maturation marker expression on CD11c(+) DCs isolated from vaccine-draining lymph nodes. Ex vivo, these DCs activate CD8(+) T cells with greater lytic capability than DC's from vaccine alone-treated neu-N mice. Finally, PTX treatment results in enhanced antigen-specific, IFN-gamma-secreting CD8(+) T cells in vivo. Thus, administration of PTX with a tumor vaccine improves T cell priming through enhanced maturation of DC. (C) 2010 Elsevier Inc. All rights reserved.
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