Suppression of intratumoral CCL22 by type I interferon inhibits migration of regulatory T cells and blocks cancer progression

  • D. A
  • M. R
  • S. E
  • et al.
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Abstract

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. Copyright © 2015 AACR.

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D., A., M., R., S., E., V.H., K., R., T., S., H., … S., E. (2015). Suppression of intratumoral CCL22 by type I interferon inhibits migration of regulatory T cells and blocks cancer progression. Cancer Research. S. Endres, Division of Clinical Pharmacology, Center of Integrated Protein Science Munich (CIPS-M), Klinikum Der Universitat Munchen, Lindwurmstrasse 2a, Munich 80337, Germany: American Association for Cancer Research Inc. (E-mail: helen.atkins@aacr.org). Retrieved from http://cancerres.aacrjournals.org/content/75/21/4483.full.pdf+html

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