Leukemia inhibitory factor protects axons in experimental autoimmune encephalomyelitis via an oligodendrocyte-independent mechanism

Melissa M Gresle, Estella Alexandrou, Qi-Zhu Wu, Gary Francis Egan, Vilija Jokubaitis, Margaret Ayers, Anna Jonas, William Doherty, Anna Friedhuber, Gerry Shaw, Michael Sendtner, Ben Emery, Trevor Kilpatrick, Helmut Butzkueven

Research output: Contribution to journalArticleResearchpeer-review

17 Citations (Scopus)

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; and whether this requires signalling through oligodendrocytes.
Original languageEnglish
Article numbere47379
Number of pages12
JournalPLoS ONE
Volume7
Issue number10
DOIs
Publication statusPublished - 2012

Cite this