期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 40, 期 12, 页码 3347-3357出版社
WILEY
DOI: 10.1002/eji.201041037
关键词
Cellular immunology; NK cells; Tumor immunology
类别
资金
- Chateaubriand scientific pre- and post-doctorate fellowships
- Nehemia-Lev-Zion excellent Ph.D scholarship
- ISEF Foundation
- Portuguese Foundation for Science and Technology (FCT)
- NIH [R01CA84232, R01CA115880]
- Institut Pasteur
- Inserm
- La Ligue Contre le Cancer
- FRM
- Israel Ministry of Health Chief Scientist's Office
- German-Israeli DIP
- Israel Academy of Sciences and Humanities
- Ministry of Science and Technology (MOST)
- German Cancer Center (DKFZ)
- EC
Chronic inflammation is associated with promotion of malignancy and tumor progression. Many tumors enhance the accumulation of myeloid-derived suppressor cells (MDSC), which contribute to tumor progression and growth by suppressing anti-tumor immune responses. Tumor-derived IL-1 beta secreted into the tumor microenvironment has been shown to induce the accumulation of MDSC possessing an enhanced capacity to suppress T cells. In this study, we found that the enhanced suppressive potential of IL-1 beta-induced MDSC was due to the activity of a novel subset of MDSC lacking Ly6C expression. This subset was present at low frequency in tumor-bearing mice in the absence of IL-1 beta-induced inflammation; however, under inflammatory conditions, Ly6C(neg) MDSC were predominant. Ly6C(neg) MDSC impaired NK cell development and functions in vitro and in vivo. These results identify a novel IL-1 beta-induced subset of MDSC with unique functional properties. Ly6C(neg) MDSC mediating NK cell suppression may thus represent useful targets for therapeutic interventions.
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