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Background  Dendritic cells (DCs) are the most potent antigen-presenting cells that link innate and adaptive immune responses, playing a pivotal role in triggering antigen-specific immunity. Antigen uptake by DCs induces maturational changes that include increased surface expression of major histocompatibility complex (MHC) and costimulatory molecules. In addition, DCs actively migrate to regional lymph nodes and activate antigen-specific naive T cells after capturing antigens. We characterize the functional changes of DCs infected with  Orientia tsutsugamushi , the causative agent of scrub typhus, since there is limited knowledge of the role played by DCs in  O. tsutsugamushi  infection.    Methodology/Principal Finding    O. tsutsugamushi  efficiently infected bone marrow-derived DCs and induced surface expression of MHC II and costimulatory molecules. In addition,  O. tsutsugamushi  induced autophagy activation, but actively escaped from this innate defense system. Infected DCs also secreted cytokines and chemokines such as IL-6, IL-12, MCP5, MIP-1α, and RANTES. Furthermore,  in vitro  migration of DCs in the presence of a CCL19 gradient within a 3D collagen matrix was drastically impaired when infected with  O. tsutsugamushi . The infected cells migrated much less efficiently into lymphatic vessels of ear dermis  ex vivo  when compared to LPS-stimulated DCs.  In vivo  migration of  O. tsutsugamushi -infected DCs to regional lymph nodes was significantly impaired and similar to that of immature DCs. Finally, we found that MAP kinases involved in chemotactic signaling were differentially activated in  O. tsutsugamushi -infected DCs.    Conclusion/Significance  These results suggest that  O. tsutsugamushi  can target DCs to exploit these sentinel cells as replication reservoirs and delay or impair the functional maturation of DCs during the bacterial infection in mammals.

Orientia tsutsugamushi Subverts Dendritic Cell Functions by Escaping from Autophagy and Impairing Their Migration