Rapidly after antigen capture and receipt of maturation signals, cDCs very transiently upregulate and then drastically downmodulate antigen up-take as well as MHC class II neosynthesis and ubiquitination. This allows efficient, selective, and long-term presentation of the antigens that cDCs have encountered at the same time of receipt of the maturation signals, while the sampling and processing of the antigens encountered after maturation is shut off. Conversely, pDCs maintain MHC class II synthesis and ubiquitination after antigen capture, allowing continous sampling of the antigenic environment for processing and presentation to CD4 T cells [118, 119] . Under conditions of systemic immune activation as occurs during infections with blood-borne pathogens, this specialization may allow pDCs to present to CD4 T cells some microbial antigens synthesized late after the initial encounter with the infectious agent, much more efficiently than cDCs. In the case of herpesviruses which are opportunistic pathogens, one could expect that cDCs are already activated by the primary infectious agents and are then impaired in their ability to respond to the secondary infection by the herpesviruses, whereas pDCs may still be efficient.