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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