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Schematic demonstration of the major findings. (1) Maturation of AML or MDS cells was stimulated by ATRA or D3 treatment and myeloid maturation could be followed by CD11b positivity. (2) ATRA- or D3-treated cells were predisposed to atypical IFN-γ signaling through STAT3 together with classical pathways such as STAT1. (3) In response to IFN-γ, CD11b+ mature AML or MDS cells more efficiently upregulated PD-1 ligands, especially PD-L1, which confer to secondary immune resistance.
