Autocrine type I IFN and contact with endothelium promote the presentation of influenza A virus by monocyte-derived APC.

摘要: Purified monocytes infected with influenza A virus do not become mature dendritic cells (DCs) and they present viral peptides poorly to autologous memory T cells. In this study, we investigated whether A-infected matured DCs a high capacity stimulate when were in model tissue setting wherein cocultured endothelium grown on type I collagen matrix. Intercellular interactions strongly promoted the Ag-presenting of monocyte-derived virus, heterologous coculture system also enhanced production IFN-alpha by absence plasmacytoid Production presence correlated monocyte differentiation their ability proliferation IFN-gamma Monocyte-derived that developed into migratory virus-specific CD4(+) CD8(+) cells, whereas those macrophages only. This onset APC activity could be partially blocked Ab IFN-alphabeta receptor UV-treated but neutralizing pathway was inconsequential live virus. Thus, IFN direct contact promote development virus-presenting which does depend However, role mediating is expendable, apparently due other mechanisms virus-mediated activation.