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Publication : PKR mediated regulation of inflammation and IL-10 during viral encephalomyelitis.

First Author  Kapil P Year  2014
Journal  J Neuroimmunol Volume  270
Issue  1-2 Pages  1-12
PubMed ID  24642385 Mgi Jnum  J:318208
Mgi Id  MGI:6858762 Doi  10.1016/j.jneuroim.2014.02.012
Citation  Kapil P, et al. (2014) PKR mediated regulation of inflammation and IL-10 during viral encephalomyelitis. J Neuroimmunol 270(1-2):1-12
abstractText  Double-stranded RNA-dependent protein kinase (PKR) regulates antiviral activity, immune responses, apoptosis and neurotoxicity. Gliatropic coronavirus infection induced PKR activation in infected as well uninfected cells within the central nervous system (CNS). However, PKR deficiency only modestly increased viral replication and did not affect IFN-alpha/beta or IL-1beta expression. Despite reduced Il-6, Ccl5, and Cxcl10 mRNA, protein levels remained unaltered. Furthermore, PKR deficiency selectively reduced IL-10 production in CD4, but not CD8 T cells, without affecting CNS pathology. The results demonstrate the ability of PKR to balance neuroinflammation by selectively modulating key cytokines and chemokines in CNS resident and CD4 T cells.
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