@article{SendtnerCarrollHoltmannetal.1994,
  author    = {Sendtner, Michael and Carroll, P. and Holtmann, B and Hughes, R. A. and Thoenen, H.},
  title     = {Ciliary Neurotrophic Factor},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42545},
  year      = {1994},
  abstract  = {No abstract available},
  language  = {en}
}
@misc{SendtnerArakawaStoecklietal.1991,
  author    = {Sendtner, Michael and Arakawa, Yoshihiro and St{\"o}ckli, Kurt A. and Kreutzberg, Georg W. and Thoenen, Hans},
  title     = {Effect of ciliary neurotrophic factor (CNTF) on motoneuron survival},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-33048},
  year      = {1991},
  abstract  = {We have demonstrated that the extensive degeneration of motoneurons in the rat facial nucleus after transection of the facial nerve in newborn rats can be prevented by local ciliary neurotrophic factor (CNTF) administration. CNTF differs distinctly from known neurotrophic molecules such as NGF, BDNF and NT-3 in both its molecular characteristics (CNTF is a cytosolic rather than a secretory molecule) and its broad spectrum of biological activities. CNTF is expressed selectively by Schwann cells and astrocytes of the peripheral and central nervous system, respectively, but not by target tissues of the great variety of CNTF -responsive neurons. CNTF mRNA is not detectable by Northern blot or PCR analysis during embryonic development and immediately after birth. However, during the second post-natal week, a more than 30-fold increase in CNTF mRNA and pro tein occurs in the sciatic nerve. Since the period of low CNTF levels in peripheral nerves coincides with that of high vulnerability of motoneurons (i.e. axonallesion results in degeneration of motoneuron cell bodies), insufficient availability of CNTF may be the reason for the rate of lesioninduced cell death of early post-natal motoneurons. Highly enriched embryonic chick motoneurons in culture are supported at survival rates higher than 60\% by CNTF, even in single cell cultures, indicating that CNTF acts directly on motoneurons. In contrast to CNTF, the members of the neurotrophin gene family (NGF, BDNF and NT-3) do not support the survival of motoneurons in culture. However, aFGF and bFGF show distinct survival activities which are additive to those of CNTF, resulting in the survival of virtually all motoneurons cultured in the presence of CNTF and bFGF.},
  language  = {en}
}
@article{GresleAlexandrouWuetal.2012,
  author    = {Gresle, Melissa M. and Alexandrou, Estella and Wu, Qizhu and Egan, Gary and Jokubaitis, Vilija and Ayers, Margaret and Jonas, Anna and Doherty, William and Friedhuber, Anna and Shaw, Gerry and Sendtner, Michael and Emery, Ben and Kilpatrick, Trevor and Butzkueven, Helmut},
  title     = {Leukemia Inhibitory Factor Protects Axons in Experimental Autoimmune Encephalomyelitis via an Oligodendrocyte-Independent Mechanism},
  series = {PLoS One},
  volume    = {7},
  journal   = {PLoS One},
  number    = {10},
  doi       = {10.1371/journal.pone.0047379},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134617},
  pages     = {e47379},
  year      = {2012},
  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. We induced MOG\(_{35-55}\) EAE in CNTF, LIF and double knockout mice. On a CNTF null background, LIF knockout was associated with increased EAE severity (EAE grade 2.1\(\pm\)0.14 vs 2.6\(\pm\)0.19; P<0.05). These mice also showed increased axonal damage relative to LIF heterozygous mice, as indicated by decreased optic nerve parallel diffusivity on MRI (1540\(\pm\)207 \(\mu\)m\(^2\)-/s vs 1310\(\pm\)175 \(\mu\)m\(^2\)-/s; P<0.05), and optic nerve (-12.5\%) and spinal cord (-16\%) axon densities; and increased serum neurofilament-H levels (2.5 fold increase). No differences in inflammatory cell numbers or peripheral auto-immune T-cell priming were evident. Oligodendrocyte-targeted gp130 knockout mice showed that disruption of CNTF/LIF signalling in these cells has no effect on acute EAE severity. These studies demonstrate that endogenous CNTF and LIF act centrally to protect axons from acute inflammatory destruction via an oligodendrocyte-independent mechanism.},
  language  = {en}
}