Crosstalk Between Dermal Fibroblasts and Dendritic Cells During Dengue Virus Infection.

摘要: Dengue virus infection (DENV-2) is transmitted by infected mosquitoes via the skin, where many dermal and epidermal cells are potentially susceptible to infection. Most of in an area will establish antiviral microenvironment control viral replication. Although cumulative studies report permissive DENV-2 dendritic cells, keratinocytes, fibroblasts, among other also infected, little information available regarding cell-to-cell crosstalk effect this on outcome Therefore, our study focused understanding contribution fibroblast cell or promotion dengue. Our results suggest that promote state over fibroblasts enhancing production type I interferon, but not proinflammatory cytokines. Infected non-infected promoted partial maturation, fibroblast-matured were less showed enhanced interferon production. We observed soluble mediators produced Poly (I:C) transfected induced allogenic T proliferation, inhibited phenomenon. Additionally, effects CD14+ monocytes analyzed assess whether they affected differentiation monocyte derived (moDC). data variable levels into even presence recombinant GM-CSF IL-4. Cells with cell-like morphology appeared culture; however, flow cytometry analysis did fully downregulate CD14 nor upregulate CD1a. revealed fibroblast-dendritic response mediated manly interferons fibroblasts. Furthermore, maturation proliferation promoted, which was DENV-2-induced mediators. Together, activation adaptive immune influenced skin resident intensity innate responses established skin.