Another negative feedback effect of IFN-I has been described in pDCs that is shared with cDCs. It relies on the IFN-I-dependent induction on DCs of the TAM receptor tyrosine kinases Axl, Tyro3, or Mer. These molecules associate with the α-chain of the IFN-I receptor and activate the suppressors of cytokine signaling-1 (SOCS-1) and SOCS-3 upon engagement by their ligands Gas6 or ProS which can themselves be produced by DCs [113] . Other cell-intrinsic mechanisms exist that also contribute to dampen pDC responses to TLR triggering, such as the engagement of the immunoreceptor tyrosinebased inhibition motif (ITIM)-bearing membrane receptor DCIR in human pDCs [114] . Interestingly, engagement of DCIR on pDCs increases their capacity to present antigen to T lymphocytes. Targeted delivery of vaccine antigens to mouse pDCs via coupling to an anti-SIGLECH antibody also promotes the induction of adaptive immune responses [115] . Thus, the mechanisms that terminate the production of innate cytokines by pDCs during responses to viral type stimuli may not only be in place to prevent the development of a cytokine shock but also to switch pDC functions towards direct activation of adaptive immunity once their initial role in the orchestration of innate immune defenses has been fulfilled.