Purpose. To examine the mechanism(s) of interferon (IFN) induced expression of major histocompatibility complex (MHC) class I molecules on the human retinoblastoma cell line, Y-79. Methods. Y-79 cells were incubated in the presence of IFN-α, -β, and -γ, Y-79 cell expression of MHC class 1 molecules was measured by flow cytometric analysis. HLA-B7 and oncogene transcription were evaluated by Northern blot analysis and nuclear runoff transcription assays. Results. IFN-γ increased MHC-class 1 antigen expression and induced a fivefold increase in its transcription rate. Posttranscriptionally, IFN-β and -γ increased steady state messenger RNA for the HLA-B7 gene. These effects were not associated with down regulation of N-myc oncogene nuclear transcription. Moreover, dexamethasone did not affect the IFN-γ induced expression of MHC-class 1 molecules. Conclusions. Both transcriptional and posttranscriptional mechanisms are implicated in the modulation of class 1 molecule expression by IFN. In addition, this modulation is not associated with down regulation of N-myc oncogene expression. Spontaneous or IFN-γ induced MHC class 1 antigen expression in retinoblastoma Y-79 cells is resistant to glucocorticoid hormones.
|Original language||English (US)|
|Number of pages||9|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Jan 1 1993|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience