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Novel GM-CSF signals via IFN-γR/IRF-1 and AKT/mTOR license monocytes for suppressor function by Eliana Ribechini, James A. Hutchinson, Sabine Hergovits, Marion Heuer, Jörg Lucas, Ulrike Schleicher, Ana-Laura Jordán Garrote, Sarah J. Potter, Paloma Riquelme, Heike Brackmann, Nora Müller, Hartmann Raifer, Ingolf Berberich, Magdalena Huber, Andreas Beilhack, Michael Lohoff, Christian Bogdan, Matthias Eyrich, Heike M. Hermanns, Edward K. Geissler, and Manfred B. Lutz BloodAdv Volume 1(14):947-960 June 13, 2017 © 2017 by The American Society of Hematology Eliana Ribechini et al. Blood Adv 2017;1:947-960 © 2017 by The American Society of Hematology GM-CSF licensing is a prerequisite to develop suppressor activity in vitro and in vivo. Eliana Ribechini et al. Blood Adv 2017;1:947-960 © 2017 by The American Society of Hematology Only classical Ly-6Chigh monocytes acquire suppressor function and NO production independent of proliferation. Eliana Ribechini et al. Blood Adv 2017;1:947-960 © 2017 by The American Society of Hematology Functionally relevant signaling intermediates contributing to GM-CSF licensing include PI3K, pAKT, pmTOR, pS6, and p4E-BP1. Eliana Ribechini et al. Blood Adv 2017;1:947-960 © 2017 by The American Society of Hematology GM-CSF licensing induces IFN-γR1/R2 assembly on the cell surface and nuclear translocation of IRF-1 required for MDSC function. Eliana Ribechini et al. Blood Adv 2017;1:947-960 © 2017 by The American Society of Hematology Induction of licensing markers in human monocytes by GM-CSF in vitro and ex vivo from tumor patients. Eliana Ribechini et al. Blood Adv 2017;1:947-960 © 2017 by The American Society of Hematology