Abstract:
:Complement is implicated in the pathology of neurodegenerative and inflammatory disease in the central nervous system (CNS). Although studies demonstrate that inhibition of complement activation attenuates disease development in the CNS, the specific complement components that contribute to the pathogenesis of CNS diseases remain unclear. To dissect the role of C5a in CNS disease, we developed a transgenic mouse that produces C5a exclusively in the brain using the astrocyte-specific, murine glial fibrillary acidic protein (GFAP) promoter. C5a/GFAP mice develop normally and do not demonstrate any signs of spontaneous inflammation or neurodegeneration with age. Using C5a/GFAP mice, we examined the outcome of the animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). To our surprise the onset and severity of myelin oligodendrocyte glycoprotein-induced EAE was essentially identical between C5a/GFAP and control mice. These results demonstrate that C5a, despite it is pro-inflammatory functions, is not critical to the development and progression of EAE.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Reiman R,Campos Torres A,Martin BK,Ting JP,Campbell IL,Barnum SRdoi
10.1016/j.neulet.2005.08.022keywords:
subject
Has Abstractpub_date
2005-12-30 00:00:00pages
134-8issue
3eissn
0304-3940issn
1872-7972pii
S0304-3940(05)00918-3journal_volume
390pub_type
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更新日期:2009-02-06 00:00:00
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