Journal article
EphA4 Receptor Tyrosine Kinase Is a Modulator of Onset and Disease Severity of Experimental Autoimmune Encephalomyelitis (EAE)
KM Munro, KJ Dixon, MM Gresle, A Jonas, D Kemper, W Doherty, LJ Fabri, CM Owczarek, M Pearse, AW Boyd, TJ Kilpatrick, H Butzkueven, AM Turnley
Plos One | PUBLIC LIBRARY SCIENCE | Published : 2013
Open access
Abstract
The EphA4 receptor tyrosine kinase is a major regulator of axonal growth and astrocyte reactivity and is a possible inflammatory mediator. Given that multiple sclerosis (MS) is primarily an inflammatory demyelinating disease and in mouse models of MS, such as experimental autoimmune encephalomyelitis (EAE), axonal degeneration and reactive gliosis are prominent clinical features, we hypothesised that endogenous EphA4 could play a role in modulating EAE. EAE was induced in EphA4 knockout and wildtype mice using MOG peptide immunisation and clinical severity and histological features of the disease were then compared in lumbar spinal cord sections. EphA4 knockout mice exhibited a markedly less..
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Funding Acknowledgements
This work was supported by a NH&MRC Project Grant #1045125 and a Multiple Sclerosis Research Australia grant. AMT is supported by an NH&MRC Fellowship, HB by an NH&MRC career development fellowship, MG by a CRE fellowship through the Melbourne Brain Centre, and KMM was supported by an NH&MRC Australian Postgraduate Research Scholarship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.