in vivo. IL6 transsignaling may also play a role in the autoimmune inflammation of the CNS, mainly by regulating the early expression of adhesion molecules, possibly via cellular networks at the BBB [71] . Ifergan et al. demonstrated that a subset of CD14 + monocytes migrate across the inflamed human BBB and differentiate into CD83 + CD209 + DCs under the influence of BBB-secreted TGFβ and granulocytemacrophage colony-stimulating factor (GM-CSF). These DCs can produce IL12p70, TGFβ, and IL6 and promote the proliferation and expansion of distinct populations of Th1 and Th17 cells. The abundance of such DCs in situ is strongly associated with microvascular BBB-ECs within acute MS lesions and with a significant number of Th17 cells in the perivascular infiltrate [72] .