A proposed model of BST2–ILT7 mediated regulation of pDC innate immune responses. (top) By sensing viral infection, pDCs can rapidly and rigorously produce large amounts of IFN-I via TLR7 or TLR9 activation. IFN-I then may induce the neighboring cells to express BST2, which in turn engages with ILT7 on pDCs to down-regulate the magnitude of IFN and cytokine responses in a negative feedback manner. (bottom) In a tumor environment where BST2 is endogenously expressed, infiltrating pDCs may be functionally suppressed to elicit normal IFN response to TLR ligands as a result of BST2–ILT7 interaction.