## Abstract ## Background and Objective Photodynamic therapy (PDT) is FDAβapproved antiβcancer modality for elimination of early disease and palliation in advanced disease. PDT efficacy depends in part on elicitation of a tumorβspecific immune response that is dependent on cytotoxic T lymphocytes
Cell type-specific regulation of major histocompatibility complex (MHC) Class I gene expression in astrocytes, oligodendrocytes, and neurons
β Scribed by Paul T. Massa; Keiko Ozato; Dale E. McFarlin
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 764 KB
- Volume
- 8
- Category
- Article
- ISSN
- 0894-1491
No coin nor oath required. For personal study only.
β¦ Synopsis
Mechanisms of major histocompatibility complex (MHC) class I gene regulation in cells of the CNS have been studied in vitro. Astrocytes in primary cultures, but neither oligodendrocytes nor neurons, constitutively expressed cell surface MHC class I molecules. Interferon-gamma (IFN-.I) treatment led to induction of MHC class I expression in astrocytes and oligodendrocytes but not in neurons. The conserved upstream sequence containing the juxtaposed nuclear factor (NF)-KB-like region I and IFN-response consensus sequence (ICS) constitutively enhanced MHC class I gene promoter activity in astrocytes, but not in oligodendrocytes or in neurons. Nuclear extracts from astrocytes, but not from oligodendrocytes and neurons, had a binding activity specific for the NF-&-like region I sequence, indicating that constitutive expression of MHC class I genes is governed by the upstream region I enhancer and its binding factor. IFN-7 treatment led to induction of MHC class I promoter activity in astrocytes and oligodendrocytes, but not in neurons. In accordance with this observation, a nuclear factor that binds to the ICS was induced in astrocytes and oligodendrocytes but not in neurons following IFN--y treatment. This study illustrates cell type-specific regulation of MHC class I genes in the CNS that correlates with the expression of DNA binding factors relevant to MHC class I gene transcription. u 1993 Wiley-Liss, Inc.
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