Considering that we found in vivo DC migration from skin to dLNs to be even more CCR7 dependent in CHS than under steady-state conditions (Fig. 1 and [Vigl et al., 2011]), a shift in the overall balance from full-length CCL21 to CCL21-ΔC during inflammation could serve to ensure in infection-induced settings that preferentially fully activated DCs—which would be expected to be CCR7hi following direct pathogen-driven maturation and to present foreign antigen—reach the dLNs. This evidence concerns the gene CCL21 and infection.