期刊
CANCER IMMUNOLOGY IMMUNOTHERAPY
卷 56, 期 1, 页码 48-59出版社
SPRINGER
DOI: 10.1007/s00262-006-0160-8
关键词
tumor immunity; tolerance; dendritic cells; regulatory T cells
资金
- NCI NIH HHS [R01 CA104926] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA104926] Funding Source: NIH RePORTER
CD4(+) CD25(+) regulatory T cells have been characterized as a critical population of immunosuppressive cells. They play a crucial role in cancer progression by inhibiting the effector function of CD4(+) or CD8(+) T lymphocytes. However, whether regulatory T lymphocytes that expand during tumor progression can modulate dendritic cell function is unclear. To address this issue, we have evaluated the inhibitory potential of CD4(+) CD25(+) regulatory T cells from mice bearing a BCR-ABL(+) leukemia on bone marrow-derived dendritic cells. We present data demonstrating that CD4(+) CD25(+) FoxP3(+) regulatory T cells from tumor-bearing animals impede dendritic cell function by downregulating the activation of the transcription factor NF-kappa B. The expression of the co-stimulatory molecules CD80, CD86 and CD40, the production of TNF-alpha, IL-12, and CCL5/RANTES by the suppressed DC is strongly down-regulated. The suppression mechanism requires TGF-beta and IL-10 and is associated with induction of the Smad signaling pathway and activation of the STAT3 transcription factor.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据