Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Logo MUG-Forschungsportal

Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid Stoffw Microb

Hochmeister, S; Pekar, T; Lindner, M; Kitic, M; Haindl, M; Storch, M; Fazekas, F; Linington, C.
Maternal neurofascin-specific autoantibodies bind to structures of the fetal nervous system during pregnancy, but have no long term effect on development in the rat.
PLoS One. 2014; 9(1):e85393-e85393 Doi: 10.1371/journal.pone.0085393 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Führende Autor*innen der Med Uni Graz
Hochmeister Sonja
Co-Autor*innen der Med Uni Graz
Fazekas Franz
Haindl Michaela Tanja
Pekar Thomas
Storch Maria

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

Neurofascin was recently reported as a target for axopathic autoantibodies in patients with multiple sclerosis (MS), a response that will exacerbate axonal pathology and disease severity in an animal model of multiple sclerosis. As transplacental transfer of maternal autoantibodies can permanently damage the developing nervous system we investigated whether intrauterine exposure to this neurofascin-specific response had any detrimental effect on white matter tract development. To address this question we intravenously injected pregnant rats with either a pathogenic anti-neurofascin monoclonal antibody or an appropriate isotype control on days 15 and 18 of pregnancy, respectively, to mimic the physiological concentration of maternal antibodies in the circulation of the fetus towards the end of pregnancy. Pups were monitored daily with respect to litter size, birth weight, growth and motor development. Histological studies were performed on E20 embryos and pups sacrificed on days 2, 10, 21, 32 and 45 days post partum. Immunohistochemistry for light and confocal microscopy confirmed passively transferred anti-neurofascin antibody had crossed the placenta to bind to distinct structures in the developing cortex and cerebellum. However, this did not result in any significant differences in litter size, birth weight, or general physical development between litters from control mothers or those treated with the neurofascin-specific antibody. Histological analysis also failed to identify any neuronal or white matter tract abnormalities induced by the neurofascin-specific antibody. We show that transplacental transfer of circulating anti-neurofascin antibodies can occur and targets specific structures in the CNS of the developing fetus. However, this did not result in any pre- or post-natal abnormalities in the offspring of the treated mothers. These results assure that even if anti-neurofascin responses are detected in pregnant women with multiple sclerosis these are unlikely to have a negative effect on their children.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Autoantibodies - metabolism
Autoantibodies - pharmacology
Cell Adhesion Molecules - antagonists & inhibitors
Disease Models, Animal -
Female -
Fetal Development - drug effects
Nerve Growth Factors - antagonists & inhibitors
Nervous System - drug effects
Nervous System - embryology
Nervous System - metabolism
Pregnancy -
Rats -

© Med Uni Graz Impressum