黑色素瘤
生物
免疫学
肿瘤微环境
癌症研究
CD8型
抗原
粒细胞巨噬细胞集落刺激因子
免疫疗法
免疫系统
肿瘤坏死因子α
癌症
抗原呈递
T细胞
细胞因子
遗传学
出处
期刊:Oncogene
[Springer Nature]
日期:2003-05-19
卷期号:22 (20): 3188-3192
被引量:162
标识
DOI:10.1038/sj.onc.1206459
摘要
The development of biochemical and genetic schemes to characterize cancer antigens led to the recognition that malignant melanoma frequently evokes a host response. While the generation of brisk T-cell infiltrates in early stage disease is correlated with prolonged survival, host reactions in most cases are insufficient to impede tumor progression. One variable that may limit the potency of the host response against nascent melanoma is the mixture of cytokines present in the tumor microenvironment. In a murine melanoma model, we identified granulocyte-macrophage colony stimulating factor (GM-CSF) as the most potent molecule for augmenting tumor immunity following gene transfer into melanoma cells. Vaccination with irradiated melanoma cells engineered to secrete GM-CSF enhances host responses through improved tumor antigen presentation by recruited dendritic cells and macrophages. Melanoma-specific CD4(+) and CD8(+) T-cells, CD1d-restricted NKT-cells, and antibodies mediate tumor rejection. Initial testing of this immunization strategy in patients with metastatic melanoma revealed the consistent induction of cellular and humoral antitumor responses that provoked the extensive necrosis of distant metastases without significant toxicity.
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