showed that in an IL-17-dependent cutaneous chronic GVHD model, donor-type F4/80+CSF-1R+ type 2 macrophages augmented cutaneous chronic GVHD in a G-CSF but not GM-CSF-dependent manner, in which the macrophages mediate fibrosis via their production of TGF-β (91). This evidence concerns the gene TGFB1 and chronic graft versus host disease.