期刊
JOURNAL OF IMMUNOLOGY
卷 174, 期 8, 页码 4880-4891出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.8.4880
关键词
-
类别
资金
- NCI NIH HHS [CA84488, CA100062] Funding Source: Medline
It is well established that tumor progression is associated with the accumulation of myeloid suppressive cells, which in mice include Gr-1(+) immature myeloid cells and F4/80(+) macrophages. The paradox is that with the exception of terminal stages of the disease or chemotherapy treatment, tumor-bearing mice or cancer patients do not display a profound systemic immune suppression. We therefore raised the question as to whether myeloid cell-mediated T cell suppression is controlled at a local level at the site of the tumor. We have demonstrated that after adoptive. transfer to tumor-bearing recipients, Gr-1(+) (immature myeloid cells) freshly isolated from spleens of tumor-bearing mice become F4/80(+) tumor-associated macrophages (TAM). These TAM, but not F4/80(+) macrophages or Gr-1(+) cells freshly isolated from spleens of tumor-bearing or naive mice were able to inhibit T cell-mediated immune response in vitro via induction of T cell apoptosis. Arginase and NO were both responsible for the apoptotic mechanism, and were seen only in TAM, but not in freshly isolated Gi1(+) cells. Using the analysis of STAT activity in combination with STAT knockout mice, we have determined that STAT1, but not STAT3 or STAT6, was responsible for TAM-suppressive activity.
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