STAT1-independent control of a neurotropic measles virus challenge in primary neurons and infected mice.
STAT1-independent control of a neurotropic measles virus challenge in primary neurons and infected mice.
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DOI：
10.4049/jimmunol.1101356
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发表时间：
2012-02-15
期刊：
影响因子：
--
通讯作者：
Rall GF
中科院分区：
文献类型：
--
作者：
O'Donnell LA;Conway S;Rose RW;Nicolas E;Slifker M;Balachandran S;Rall GF
Neurons are chiefly non-renewable; thus, cytolytic immune strategies to clear or control neurotropic viral infections could have lasting neurological consequences. Interferon-gamma (IFNγ) is a potent anti-viral cytokine that is critical for non-cytolytic clearance of multiple neurotropic viral infections, including measles virus (MV); however, the downstream pathways through which IFNγ functions in neurons have not been defined. Unlike most cell types studied to date in which IFNγ affects gene expression via rapid and robust activation of STAT1, basal STAT1 levels in primary hippocampal neurons are constitutively low, resulting in attenuated STAT1 activation and consequently slower kinetics of IFNγ–driven STAT1-dependent gene expression. Given this altered expression and activation of STAT1 in neurons, we sought to determine whether STAT1 was required for IFNγ-mediated protection from infection in neurons. To do so, we evaluated the consequences of MV challenge of STAT1-deficient mice and primary hippocampal neurons explanted from these mice. Surprisingly, the absence of STAT1 did not restrict the ability of IFNγ to control viral infection either in vivo or ex vivo. Moreover, the canonical IFNγ-triggered STAT1 gene expression profile was not induced in STAT1-deficient neurons, suggesting that IFNγ regulates neuronal STAT1-independent pathways to control viral replication.
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5.4
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Lawrence, DMP;Patterson, CE;Rall, GF
通讯作者：
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