@entity2803 retinal pigment epithelial cells by anti-pp65 XXXX (+) cytotoxic T cells.

@entity2803 @entity8680 @entity281 @entity4538 @entity816 @entity405
PURPOSE: Host defense against @entity281 by @entity4538 ) is ensured in great part by cytotoxic @entity405 (+) T lymphocytes (CTLs) directed against the tegument protein pp65. The hyperimmediate release of incoming pp65 into the major histocompatibility complex (MHC) class I pathway after fusion of the virus with the cell membrane provides a very early mechanism of defense. In retinal pigment epithelial (RPE) cells HCMV is known to enter through endocytosis. This study was conducted to determine whether this means of penetration into the cells would allow the virus to elude immune surveillance. METHODS: Infection of RPE cells with HCMV AD169 was performed for 6 hours, 48 hours, and 8 days. Expression of intracellular pp65 in RPE cells and in the @entity816 reference cell line U373MG was evaluated by flow cytometry, fluorescence microscopy, and Western blot analysis. Killing of both @entity2803 cell lines by HLA-A2-restricted @entity405 (+) CTLs directed against pp65 was monitored by @entity8680 -release assays. RESULTS: RPE cells were not lysed by CTLs directed against incoming pp65, contrary to U373MG. Moreover, both cell lines were not killed by anti-pp65 CTLs later after @entity281 , because of the MHC class-I-downregulating effect of HCMV unique short (US2-11) proteins. CONCLUSIONS: In RPE cells, both HCMV entry through endocytosis and the immunosuppressive effect of US proteins could allow the virus to evade immune surveillance at any stage of @entity281 , which could promote viral spreading within the retina.
