Journal article
Leukemia Inhibitory Factor Protects Axons in Experimental Autoimmune Encephalomyelitis via an Oligodendrocyte-Independent Mechanism
MM Gresle, E Alexandrou, Q Wu, G Egan, V Jokubaitis, M Ayers, A Jonas, W Doherty, A Friedhuber, G Shaw, M Sendtner, B Emery, T Kilpatrick, H Butzkueven
Plos One | PUBLIC LIBRARY SCIENCE | Published : 2012
Open access
Abstract
Leukemia inhibitory factor (LIF) and Ciliary Neurotrophic factor (CNTF) are members of the interleukin-6 family of cytokines, defined by use of the gp130 molecule as an obligate receptor. In the murine experimental autoimmune encephalomyelitis (EAE) model, antagonism of LIF and genetic deletion of CNTF worsen disease. The potential mechanism of action of these cytokines in EAE is complex, as gp130 is expressed by all neural cells, and could involve immuno-modulation, reduction of oligodendrocyte injury, neuronal protection, or a combination of these actions. In this study we aim to investigate whether the beneficial effects of CNTF/LIF signalling in EAE are associated with axonal protection;..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
This work was supported by the National Multiple Sclerosis Society (United States of America) [Project Grant RG3850A3/1 to HB and TK]; National Health and Medical Research Council Australia [Project Grant 509088 to HB and TK, and Career Development Award to HB]; Melbourne Brain Centre at RMH [CRE fellowship to MG]. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.