Neuron-specific regulation of major histocompatibility complex class I, interferon-β, and anti-viral state genes

• Published in: Journal of neuroimmunology 1995-05, Vol.58 (2), p.145-155
• Main Authors: Ward, Laurie A., Massa, Paul T.
• Format: Article
• Language: English
• Subjects: 3T3 Cells; Animals; Astrocytes; Astrocytes - metabolism; Base Sequence; Genes; Histocompatibility Antigens Class I - genetics; Histocompatibility Antigens Class I - metabolism; Interferon-beta - genetics; Interferon-beta - metabolism; Interferon-β; Major histocompatibility complex class I; Mice; Molecular Sequence Data; Neurons; Neurons - metabolism; Neurons - virology; Parainfluenza Virus 1, Human - metabolism; Poly I-C - metabolism; Virus
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/0165-5728(95)00005-M

The regulation of major histocompatibility complex (MHC) class I, interferon (IFN)-β, and anti-viral state expression in neurons was analyzed. Treatment of neurons with either double-stranded RNA (poly I:poly C) or virus, but not IFNs, induced high levels of IFN-β, but not MHC class I genes. However, neurons treated with IFN-β established an anti-viral state. Transfection of neurons with IFN-β constructs showed that a region containing PRDI (IRF-E site) and PRDII ( κB site) mediated induction, but closely related sites in a MHC class I construct did not. Gel mobility shift assays indicated that transcription factors containing the RelA (p65) component of NF- κB, but not p50, bound to PRDII. PRDI, however, bound to transcriptional antagonist IRF-2. Unique selective induction of these transcription factors is likely to mediate non-coordinate expression of IFN-β, MHC class I, and anti-viral state genes in neurons.