Dengue virus inhibits the production of type I interferon in primary human dendritic cells.
Dengue virus (DENV) infects human immune cells in vitro and likely infects dendritic cells (DCs) in vivo. DENV-2 productive infection induces activation and release of high levels of chemokines and proinflammatory cytokines in monocyte-derived DCs (moDCs), with the notable exception of alpha/beta interferon (IFN-alpha/beta). Interestingly, DENV-2-infected moDCs fail to prime T cells, most likely due to the lack of IFN-alpha/beta released by moDCs, since this effect was reversed by addition of exogenous IFN-beta. Together, our data show that inhibition of IFN-alpha/beta production by DENV in primary human moDCs is a novel mechanism of immune evasion.
Rodriguez-Madoz
Juan R
JR
Department of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1124, New York, NY 10029, USA.
Bernal-Rubio
Dabeiba
D
Kaminski
Dorota
D
Boyd
Kelley
K
Fernandez-Sesma
Ana
A
D002478:Cells, Cultured; D003713:Dendritic Cells / Q000276:immunology* / Q000821:virology*; D003716:Dengue Virus / Q000276:immunology* / Q000472:pathogenicity*; D006801:Humans; D007370:Interferon Type I / Q000037:antagonists & inhibitors*; D008213:Lymphocyte Activation; D013601:T-Lymphocytes / Q000276:immunology
D007370:Interferon Type I