CCR7 plays a dual role in DCs mobilization, promoting chemotaxis and docking to lymphatics. After s.c. injection of LPS-activated CFSE-stained BMDCs to the footpad, WT DCs (a–c) moved linearly toward an initial lymphatic, compatible with chemotaxis. DCs that crossed the endothelium clustered in the proximal sections of initial lymphatics, either in blind ends (c, left rectangle) or in adjacent sections (c, right rectangle). (d) Within 24 h, WT cells have efficiently entered lymphatics. In contrast, CCR7^−/− cells (e) kept crawling in the interstitium bypassing the lymphatic vessels they encountered (four representative cells tracked), suggesting that CCR7 promotes DC adhesion to lymphatics. This pattern was also apparent (f) when both WT and CCR7^−/− DCs were co-injected. CCR7^−/− DCs crawled as fast as WT DCs in the dermis (P = 0.29; g) but were less persistent (P = 0.006; h), implying that CCR7 ligation is not essential for DC chemokinesis but participates in their chemotaxis. Persistence index was calculated by dividing the cell displacement by path length. Data points represent individual cells and were pooled from three mice for each condition. Red bars denote the mean. *, P = 0.006. (i) When BMDCs were co-injected with CCL21, their migration to the popliteal LN was not affected, indicating that misplaced chemokine did not misguide DCs and prevent random migration and docking on endothelial CCL21. Data indicate the percentage of injected DCs out of resident LN CD11c⁺ cells. Error bars denote SEM.