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MV infection of DCs likely contributes to functional deficiency in these cells; therefore playing a role in MV\u2010induced immunosuppression. DCs appeared to mature phenotypically; however, the ability of infected cells to stimulate T cells was compromised. Phenotypic maturation of infected immature DCs was partially controlled by IFN production; however, infected DCs also maintained markers of an immature phenotype such as the continued uptake of antigen and lack of expression of chemokine receptor CCR7. Furthermore, mature DCs did not appear to maintain phenotypic maturation following infection demonstrated by decreased MHC and co\u2010stimulatory molecule expression. Several mechanisms of MV\u2010induced DC dysfunction have been suggested, each likely contributing to the immunosuppressive effect of MV\u2010infected DCs. Infected DCs responded aberrantly to secondary maturation stimuli such as CD40L or TLR4 stimulation. MV infection resulted in apoptosis in DC\/T\u2010cell cocultures, which may contribute to a reduced T\u2010cell response. Additionally, the immunological synapse between infected DCs and T cells was compromised resulting in reduced T\u2010cell interaction times and activation signaling. The mechanisms of MV contribution to DC dysfunction appear multifaceted and central to MV\u2010induced immunosuppression. Published 2012. 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