Inhibition of dendritic cell maturation by herpes simplex virus.
Maturation of dendritic cells (DC), leading to migration and increased T cell stimulatory capacity, is essential for the initiation of immune responses. This process is triggered by a variety of stimuli, such as inflammatory cytokines, bacterial and viral products. Using a recombinant disabled infectious single cycle herpes simplex virus 1 (HSV-1) encoding green fluorescent protein, we show that the infected DC are defective in up-regulating co-stimulatory molecules, do not produce cytokines, and do not acquire responsiveness to chemokines required for migration to secondary lymphoid organs. These results reveal yet another strategy used by HSV-1 to evade the immune response, namely the inhibition of signaling pathways involved in DC maturation.
Salio
M
M
Basel Institute for Immunology Basel, Switzerland. salio@bii.ch
Cella
M
M
Suter
M
M
Lanzavecchia
A
A
D015815:Cell Adhesion Molecules; D002454:Cell Differentiation / Q000276:immunology; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000276:immunology* / Q000821:virology; D018259:Herpesvirus 1, Human / Q000276:immunology* / Q000472:pathogenicity; D006801:Humans; D016753:Interleukin-10 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008213:Lymphocyte Activation; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D000075983:Nectins; D018124:Receptors, Tumor Necrosis Factor; D053240:Receptors, Tumor Necrosis Factor, Member 14; D011991:Receptors, Virus / Q000096:biosynthesis; D013601:T-Lymphocytes / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D015815:Cell Adhesion Molecules; D015850:Interleukin-6; D008562:Membrane Glycoproteins; D000075983:Nectins; D018124:Receptors, Tumor Necrosis Factor; D053240:Receptors, Tumor Necrosis Factor, Member 14; D011991:Receptors, Virus; C506028:TNFRSF14 protein, human; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10