Brain Advance Access published online on February 20, 2008
Brain, doi:10.1093/brain/awn028
© The Author (2008). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
CNTF, a key factor mediating the beneficial effects of inflammatory reactions in the eye
Department of Experimental Neurology, University of Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany
Correspondence to:
E-mail: dietmar.fischer@uni-ulm.de
| The first 150 words of the full text of this article appear below. |
Sir, retinal ganglion cells (RGCs) are normally unable to regenerate axons. However, they can be transformed into a robust regenerative state by lens injury (LI) or by intravitreal injections of either lens-derived β-/
-crystallins or zymosan (Fischer et al., 2000
, 2001, 2004, 2008; Leon et al., 2000). Based on evidence provided in Müller et al. (2007) and the literature, we propose that astrocyte-derived CNTF and activation of its major downstream signalling pathway in RGCs, the JAK/STAT3 pathway, are both essentially involved in switching these neurons to an active regenerative state after LI. By arguing against a role of CNTF and JAK/STAT3 signalling in this context, Benowitz and colleagues have ignored important evidence in the literature and also presented data from our own and other groups inaccurately, as described later.
The literature contains compelling evidence that CNTF directly stimulates axon regeneration of