IFNbeta inhibits DC migration in vitro and in vivo (92.2)

TL;DRAbstract

Abstract Interferon β (IFN β) is a widely approved therapeutic option for the treatment of multiple sclerosis (MS)/experimental autoimmune encephalomyelitis (EAE). However, the molecular mechanisms underlying the effects of IFNβ in MS/EAE are still not fully understood. In EAE, the major players are encephalitogenic CD4+ T cells and perivascular myeloid dendritic cells (DC). Therefore, migration of both peripheral T cells and DC into the CNS is essential for development of EAE/MS. Migration of DC from the inflammatory site to draining lymph nodes for antigen presentation and activation of naïve T cells, and to the CNS during chronic neuroinflammation requires CCR7 and MMP-9 expression. In this study, we report for the first time that IFNβ inhibits CCR7 expression and MMP-9 production in DC matured with a cytokine cocktail (TNFα+IL-1+IL-6+PGE2). In addition, DC matured in the presence of IFNβ exhibit a lower migratory capacity compared to mature DC. STAT-1 signaling is essential for IF

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