Respiratory syncytial virus infection of human respiratory epithelial cells up-regulates class I MHC expression through the induction of IFN-beta and IL-1 alpha.

摘要: CD8+ T cells mediate some of the damage to lung epithelium following respiratory syncytial virus (RSV) infection. Since recognize antigen-laden class I MHC molecules on target cells, we examined in this study expression by RSV-infected epithelial cells. Respiratory cell lines and bronchial from normal human tissue responded RSV infection with an increased as determined flow cytometry immunoprecipitation metabolically radiolabeled The increase was dependent infectious, replicating virus. UV-irradiated culture supernatants A549 when added fresh cultures, induced those increasing activity within due, large part, IFN-beta, a lesser extent IL-1 alpha. addition neutralizing Abs both cytokines completely blocked treated above-mentioned supernatants. These results demonstrate that elicits IFN-beta production which turn leads their synthesis MHC, would facilitate recognition lysis RSV-specific