Importantly, the capacity of WT and pearl CD11c+ DCs to mature (assessed by up-regulation of the costimulatory molecules CD40 and CD86) and their migratory potential (assessed by up-regulation of CCR7, responsible for DC homing to T cell areas of lymph nodes and spleen; [31, 32]) in response to STm infection ex vivo did not significantly differ (S1C and S1D Fig and ref. [18]), in agreement with the similar DC percentages in those tissues. The gene discussed is CCR7; the disease is infection.