Neuron-specific regulation of major histocompatibility complex class I, interferon-beta, and anti-viral state genes.
The regulation of major histocompatibility complex (MHC) class I, interferon (IFN)-beta, 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-beta, but not MHC class I genes. However, neurons treated with IFN-beta established an anti-viral state. Transfection of neurons with IFN-beta constructs showed that a region containing PRDI (IRF-E site) and PRDII (kappa B 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-kappa B, 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-beta, MHC class I, and anti-viral state genes in neurons.
Ward
L A
LA
Neuroscience Program, State University of New York Health Science Center at Syracus 13210, USA.
Massa
P T
PT
D016475:3T3 Cells; D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D001483:Base Sequence; D005796:Genes; D015395:Histocompatibility Antigens Class I / Q000235:genetics / Q000378:metabolism*; D016899:Interferon-beta / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008969:Molecular Sequence Data; D009474:Neurons / Q000378:metabolism* / Q000821:virology; D010222:Parainfluenza Virus 1, Human / Q000378:metabolism; D011070:Poly I-C / Q000378:metabolism
D015395:Histocompatibility Antigens Class I; D016899:Interferon-beta; D011070:Poly I-C