期刊
CANCER RESEARCH
卷 75, 期 21, 页码 4483-4493出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-14-3499
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类别
资金
- LMUexcellent research professorship
- Friedrich Baur Foundation
- Deutsche Forschungsgemeinschaft Graduiertenkolleg [1202]
- DFG [AN 801/2-1]
- Deutsche Krebshilfe [111326]
- excellence cluster [CIPS-M 114]
- BayImmuNet
- Swiss National Science Foundation [138284, 156372]
- Krebsforschung Schweiz [2910-02-2012]
The chemokine CCL22 is abundantly expressed in many types of cancer and is instrumental for intratumoral recruitment of regulatory T cells (Treg), an important subset of immunosuppressive and tumor-promoting lymphocytes. In this study, we offer evidence for a generalized strategy to blunt Treg activity that can limit immune escape and promote tumor rejection. Activation of innate immunity with Toll-like receptor (TLR) or RIG-I-like receptor (RLR) ligands prevented accumulation of Treg in tumors by blocking their immigration. Mechanistic investigations indicated that Treg blockade was a consequence of reduced intratumoral CCL22 levels caused by type I IFN. Notably, stable expression of CCL22 abrogated the antitumor effects of treatment with RLR or TLR ligands. Taken together, our findings argue that type I IFN blocks the Treg-attracting chemokine CCL22 and thus helps limit the recruitment of Treg to tumors, a finding with implications for cancer immunotherapy. (C) 2015 AACR.
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