Mechanisms responsible for keeping the pDC in this state include the secretion of prostaglandin 2 (PGE2) and TGF-β, which, in a synergistic manner inhibit pDC-derived IFN-α and TNF-α production in response to TLR7 and 9 ligands, as well as inhibiting CCR7 expression, thereby impairing the migration of pDCs to the tumor-draining LN to prime T cells with tumor antigens (148–150). Here, CCR7 is linked to neoplasm.