IL10 and infection: Despite poor, or relatively low expression of surface markers associated with the potential capacity of DCs to activate or promote the activation of T cells, a common feature that has been repeatedly observed in hRSV-infected DCs is the secretion of cytokines that may promote the differentiation of T cells into phenotypes that are not favorable for the effective resolution of infection, such as IL-6 and IL-10, which lead to Th2 CD4+ T cell responses (66, 81).