期刊
CANCER RESEARCH
卷 72, 期 14, 页码 3664-3676出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-11-2791
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类别
资金
- Swiss National Science Foundation
- Swiss Cancer League
- Bernese Cancer League
- Berger Janser Stiftung
- Swiss MD-PhD scholarship
- Gertrud Hagmann Stiftung
- SwissLife-Jubilaumsstiftung
- Sassella Foundation
- Ehmann Stiftung
- Fondazione per la ricerca sulla trasfusione e sui trapianti
- Olga-Mayenfisch-Stiftung
Signaling of the TNF receptor superfamily member CD27 activates costimulatory pathways to elicit T- and B-cell responses. CD27 signaling is regulated by the expression of its ligand CD70 on subsets of dendritic cells and lymphocytes. Here, we analyzed the role of the CD27-CD70 interaction in the immunologic control of solid tumors in Cd27-deficient mice. In tumor-bearing wild-type mice, the CD27-CD70 interaction increased the frequency of regulatory T cells (Tregs), reduced tumor-specific T-cell responses, increased angiogenesis, and promoted tumor growth. CD27 signaling reduced apoptosis of Tregs in vivo and induced CD4(+) effector T cells (Teffs) to produce interleukin-2, a key survival factor for Tregs. Consequently, the frequency of Tregs and growth of solid tumors were reduced in Cd27-deficient mice or in wild-type mice treated with monoclonal antibody to block CD27 signaling. Our findings, therefore, provide a novel mechanism by which the adaptive immune system enhances tumor growth and may offer an attractive strategy to treat solid tumors. Cancer Res; 72(14); 3664-76. (C)2012 AACR.
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