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IL-27 confers a protumorigenic activity of regulatory T cells via CD39

Young-Jun Park1,2, Heeju Ryu1,2, Garam Choi1,2

  • 1Laboratory of Immune Regulation, Research Institute of Pharmaceutical Sciences, Seoul National University, 151-742 Seoul, Republic of Korea.

Proceedings of the National Academy of Sciences of the United States of America
|February 6, 2019
PubMed

Expression of ectonucleotidase CD39 contributes to the suppressive activity of Foxp3+ regulatory T cells (Tregs) by hydrolyzing immunogenic ATP into AMP. The molecular mechanism that drives CD39 expression on Tregs remains elusive. We found that tumor-infiltrating Tregs (Ti-Tregs) failed to up-regulate CD39 in mice lacking EBI3 subunit of IL-27 or IL-27Ra. Mixed bone marrow chimera and in vitro studies showed that IL-27 signaling in Tregs directly drives CD39 expression on Ti-Tregs in a STAT1-dependent, but STAT3- and T-bet-independent, manner. Tregs stimulated with IL-27 showed enhanced suppressive activities against CD8+ T cell responses in vitro. Moreover, IL-27Ra-deficient Tregs and STAT1-deficient Tregs were less efficient than WT Tregs in suppressing antitumor immunity in vivo. CD39 inhibition significantly abolished IL-27-induced suppressive activities of Tregs. Thus, IL-27 signaling in Tregs critically contributes to protumorigenic properties of Tregs via up-regulation of CD39.

Keywords:
CD39IL-27STAT1regulatory T celltumor immunity

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