Our results show that, during both in vitro (data not shown) and in vivo infections, CCR4−/− DCs exhibited decreased expression of MHC class II and the co-stimulatory molecule CD86 as well as increased expression of the inhibitory molecule PD-L1, indicating that CCR4 is important for the activation of DCs after CVB5 infection. The gene discussed is CCR4; the disease is infection.