GFI1/HDAC1‐axis differentially regulates immunosuppressive CD73 in human tumor‐associated FOXP3 ⁺ Th17 and inflammation‐linked Th17 cells

Plasticity between Th17 and Treg cells is regarded as a crucial determinant of tumor-associated immunosuppression. Classically mediate inflammatory responses through production cytokine IL17. Recently, have also been shown to acquire suppressive phenotypes in tumor microenvironment. However, the mechanism by which they such immunosuppressive properties still elusive. Here, we report that microenvironment cell acquires expressing lineage-specific transcription factor FOXP3 ectonucleotidase CD73. We designate this Th17reg perceive property dependent on It was observed classical cell, GFI1 recruits HDAC1 change euchromatin into tightly-packed heterochromatin at proximal-promoter region CD73 repress its expression. Whereas cannot get access CD73-promoter due state binding site and, thus, recruit HDAC1, failing suppress expression