Suppression of intratumoral CCL22 by type I interferon inhibits migration of regulatory T cells and blocks cancer progression
- Anz, David Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Rapp, Moritz Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Eiber, Stephan Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Koelzer, Viktor H Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Thaler, Raffael Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Haubner, Sascha Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Knott, Max Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Nagel, Sarah Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Golic, Michaela Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Wiedemann, Gabriela M Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Bauernfeind, Franz Department of Clinical Pharmacology and Clinical Chemistry, University of Bonn, Germany
- Wurzenberger, Cornelia Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Hornung, Veit Department of Clinical Pharmacology and Clinical Chemistry, University of Bonn, Germany
- Scholz, Christoph Department of Obstetrics and Gynecology, Ulm University Medical Centre, Germany
- Mayr, Doris Pathology, Ludwig-Maximilians-Universität, Germany
- Rothenfusser, Simon Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Endres, Stefan Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany
- Bourquin, Carole Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Germany - Medicine Department, University of Fribourg, Switzerland
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02.10.2015
Published in:
- Cancer Research. - 2015, vol. 75, no. 21, p. 4483-4493
English
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 Treg blockade was a consequence of reduced intratumoral CCL22 levels caused by type I interferon. Notably, stable expression of CCL22 abrogated the antitumor effects of treatment with RLR or TLR ligands. Taken together, our findings argue that type I interferon blocks the Treg-attracting chemokine CCL22 and thus helps limit the recruitment of Treg to tumors, a finding with implications for cancer immunotherapy.
- Faculty
- Faculté des sciences et de médecine
- Department
- Département de Médecine
- Language
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- English
- Classification
- Biological sciences
- License
- License undefined
- Identifiers
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- RERO DOC 257508
- DOI 10.1158/0008-5472.CAN-14-3499
- Persistent URL
- https://folia.unifr.ch/unifr/documents/304750
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