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Modulation of major histocompatibility complex class 1 genes in human retinoblastoma cells by interferons.

作者信息

Barez S, Boumpas D T, Percopo C M, Anastassiou E D, Hooks J J, Detrick B

机构信息

Immunology and Virology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.

出版信息

Invest Ophthalmol Vis Sci. 1993 Aug;34(9):2613-21.

PMID:7688356
Abstract

PURPOSE

To examine the mechanism(s) of interferon (IFN) induced expression of major histocompatibility complex (MHC) class 1 molecules on the human retinoblastoma cell line, Y-79.

METHODS

Y-79 cells were incubated in the presence of IFN-alpha, -beta, and -gamma. 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-gamma increased MHC-class 1 antigen expression and induced a fivefold increase in its transcription rate. Posttranscriptionally, IFN-beta and -gamma 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-gamma 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-gamma induced MHC class 1 antigen expression in retinoblastoma Y-79 cells is resistant to glucocorticoid hormones.

摘要

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