Dendritic cells (DC) play an essential role in the initiation and regulation of immune responses. Therefore, it is of pivotal interest to understand the interaction of this type of cells with pathogens. DC have been shown to take up invading pathogens or pathogen-derived antigens and transport these to inductive sites of the immune system. There, they efficiently present such antigens to T cells [1]. In order to fulfil this task, DC are equipped to phagocytose microorganisms or infected cells and start a sequence of differentiation steps that involves mobilization and migration as well as processing and efficient presentation of antigens. This sequence of events can be set off by pro-inflammatory cytokines produced by cells in the infected tissue or by properties of the pathogens themselves [1].

Many pathogens have acquired escape mechanisms that block the efficient induction of immune responses. Thus, bacteria have been reported to modulate MHC class II presentation by interference with the antigen processing compartments. For example, mycobacteria have been demonstrated to inhibit endosomal acidification and class II presentation as well as to downregulate MHC class II expression. Down-regulation of co-stimulatory molecules has also been shown [2, 3]. In addition, Listeria monocytogenes have been reported to inhibit CD4 T cell responses by inducing an antigenspecific antagonism in murine APC [4]. Furthermore, lis-