Journal of Virology · 2018 · 28 citations · 62 references
Life SciencesImmunologyInfectious DiseasesCancer ImmunologyInnate ImmunityMolecular ImmunologyAntiviral ImmunityInnate Immune ReceptorsInnate Immune RecognitionInnate Immune ResponseInnate Immune Signaling PathwaysToll-like ReceptorsAntiviral Innate Immune SignalingAntiviral Innate SignalingEndosomal Toll-like Receptor SignalingEndosomal Toll-like ReceptorsHost Antiviral ResponseInnate Immunity PathwaysToll-like Receptor SignalingToll-like Receptors In Cancer
The two human gammaherpesviruses, Epstein-Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV), can cause aggressive forms of cancer. These herpesviruses are strictly host specific, and therefore the homolog murine gammaherpesvirus 68 (MHV68) is a widely used model to obtain in vivo insights into the interaction between these two gammaherpesviruses and their host. Like EBV and KSHV, MHV68 establishes lifelong latency in B cells. The innate immune system serves as one of the first lines of host defense, with pattern recognition receptors such as the Toll-like receptors playing a crucial role in mounting a potent antiviral immune response to various pathogens. Here, we shed light on a yet unanticipated role of Toll-like receptor 7 in the recognition of MHV68 in a subset of immune cells called plasmacytoid dendritic cells, as well as on the control of this virus in its host.
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