Similar to human measles clinical findings in canine distemper virus -infected dogs include fever, rash, respiratory signs, and lymphopenia. Affected animals are prone to opportunistic infections as a consequence of generalized lymphoid depletion and profound immunosuppression. Moreover, persistent infection of peripheral lymphoid organs and the central nervous system of carnivores leads to long lasting immune alterations and immune mediated neuropathology. Dendritic cells represent the most potent antigen presenting cell population, which initiate primary T cell responses and play an important role also for B cell immunity. Several pathogens, including human herpesvirus type-1 as well as human and feline immunodeficiency viruses, target DCs and have evolved strategies to modulate their cytokine expression and antigen presenting capacity, thereby promoting virus immune evasion and persistence. Other mechanisms include alteration of endocytosis, vesicle trafficking, and immunological synapse formation or apoptosis induction of infected DCs. A disturbed function of antigen presenting cells, including DCs, is supposed to contribute to immunosuppression in measles patients. Moreover, following infection of the respiratory tract, MV-infected DCs might mediate virus transmission to secondary lymphoid organs. During the chronic disease stage of canine distemper, cells with a DC-like morphology seem to serve as the primary host cells for the virus, which might promote viral persistence in lymphoid organs. Thus, an inhibited terminal differentiation of DCs is currently discussed to be responsible for diminished antigen presenting function and disturbed repopulation of lymphoid tissues in CDV-infected dogs, as suggested for MV-infection. In addition, CDV-infection of thymic DCs may result in compromised T cell maturation, promoting the release of immature, potentially autoreactive lymphocytes, demonstrating a potential participation of DCs in both CDV-induced immunosuppression and immunopathology. However, whether CDV has the ability to infect canine DCs and direct viral effects upon these professional antigen presenting cells have not yet been confirmed. The aim of the present study was to determine the permissiveness of canine DCs to CDV in vitro. Besides antigen presentation via the major histocompatibility complex, adequate T cell activation by DCs requires co-stimulation by molecules such as CD80 and CD86. An additional signal is mediated by DC-released cytokines leading to T cell polarization. Thus, in order to testify the hypothesis that infection leads to an impaired T cell stimulatory capacity of these cells, the impact of CDV upon molecules involved in antigen presentation and co-stimulation and the associated cytokine expression was investigated. The present study demonstrates the ability of CDV to infect canine DCs and to modulate their antigen presenting properties and cytokine expression.