Abstract

Abstract Although immune mechanisms can suppress tumor growth, tumors establish potent and overlapping mechanisms that mediate immune evasion. Emerging evidence suggests a link between tumor immune tolerance and angiogenesis. Hypoxia, a condition known to drive tumor angiogenesis, results in release of damage-associated molecular pattern molecules, which can trigger tumor immune rejection. Thus, counter-activation of tolerance mechanisms at the site of tumor hypoxia would be a critical condition to maintain immunologic escape of tumors. However, a direct link between tumor hypoxia and tolerance through the recruitment of regulatory cells has not been established. We hypothesized that tumor hypoxia induces expression of chemotactic factors promoting tolerance. Here we show that tumor hypoxia promotes T regulatory (Treg) cell recruitment via the CCL28 chemokine, which in turn promotes tumor tolerance and angiogenesis. Thus, peripheral immune tolerance and angiogenesis are intimately connected and cooperate to sustain tumor growth. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 308. doi:1538-7445.AM2012-308

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