Dendritic cell (DC) precursors enter inflammatory and cancerous lesional sites where they are instructed to acquire specific phenotypic and functional characteristics. We recently observed that bone morphogenetic protein (BMP)-7 and BMP downstream signaling is strongly upregulated in psoriatic epithelial lesions in human patients and in the keratinocyte-specific cjun/junB mouse model. Additionally, another member of the TGF-b/BMP family, TGF-b1 can be detected at these sites. Both BMP7 and TGF-b1 can signal through BMPR1a/ALK3-SMAD1/5/8 to promote epidermal Langerhans cell (LC) differentiation from human progenitor cells and blood cDC2s. BMPR1a was specifically required in murine CD11c+ DCs for resolving established psoriatic skin lesions and for promoting lesional regulatory T cell (Treg) frequencies. We extended our studies to a recently established in vitro model of BRAFV600e oncogene-driven Langerhans cell histiocytosis (LCH). Monoallelic BRAFV600e carrying progenitor cells exhibited augmented BMP receptor signaling. They showed regulatory DC characteristics and possessed Treg stimulatory capacity. Specific interference with BMP signaling abrogated LCH cell differentiation. Immunohistology studies of BRAFV600e positive LCH cells confirmed observations from the in vitro model. In conclusion, BMP signaling promotes regulatory DC characteristics in psoriatic skin inflammation and oncogene-driven histiocytosis.