Journal article

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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
  • English
Classification
Biology
License
License undefined
Identifiers
Persistent URL
https://folia.unifr.ch/unifr/documents/304750
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