Hostile communication of measles virus with host innate immunity and dendritic cells.
Following measles virus (MV) infection, host innate immune responses promptly operate to purge the virus. Detection of alerting measles viral components or replication intermediates by pattern-recognizing host machinery of Toll-like receptors and RNA helicases triggers signaling to synthesize array of anti-viral and immunoregulatory molecules, including type I interferon (IFN). Diverse subtypes of dendritic cells (DCs) play pivotal roles in both host innate immunity on the primary MV-infected site and initiating adaptive immune responses on secondary lymphoid tissues. Responding to the predictable host immune responses, MV appears to have devised multiple strategies to evade, suppress, or even utilize host innate immunity and DC responses. This review focuses on versatile actions of MV-induced type I IFNs causing beneficial or deleterious influence on host immunity and the interplay between MV and heterogeneous DCs at distinct locations.
Hahm
B
B
Department of Surgery, Center for Cellular and Molecular Immunology, University of Missouri-Columbia School of Medicine, One Hospital Dr., Columbia, MO 65212, USA. hahmb@health.missouri.edu
D000818:Animals; D003713:Dendritic Cells / Q000276:immunology* / Q000821:virology; D054884:Host-Pathogen Interactions; D006801:Humans; D007113:Immunity, Innate; D007370:Interferon Type I / Q000276:immunology; D008457:Measles / Q000276:immunology* / Q000503:physiopathology / Q000821:virology; D008459:Measles virus / Q000276:immunology*; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000276:immunology
D007370:Interferon Type I; D051193:Toll-Like Receptors