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  Cytotoxic potential of proinflammatory cytokines: combined deletion of TNF receptors TNFR1 and TNFR2 prevents motoneuron cell death after facial axotomy in adult mouse

Raivich, G., Liu, Z. Q., Kloss, C. U. A., Labow, M., Bluethmann, H., & Bohatschek, M. (2002). Cytotoxic potential of proinflammatory cytokines: combined deletion of TNF receptors TNFR1 and TNFR2 prevents motoneuron cell death after facial axotomy in adult mouse. Experimental Neurology, 178(2), 186-193. doi:10.1006/exnr.2002.8024.

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 Creators:
Raivich, G.1, Author           
Liu, Z. Q.1, Author           
Kloss, C. U. A.1, Author           
Labow, M.2, Author
Bluethmann, H.2, Author
Bohatschek, M.1, Author           
Affiliations:
1Emeritus Group: Neuromorphology / Kreutzberg, MPI of Neurobiology, Max Planck Society, ou_1113551              
2Univ Coll London, Dept Anat, Dept Obstet & Gynaecol, Perinatal; Brain Repair Grp, 86-96 Chenies Mews, London WC1E 6HX, England; Univ Coll London, Dept Anat, Dept Obstet & Gynaecol, Perinatal Brain Repair Grp, London WC1E 6HX, England; F Hoffmann La Roche & Co Ltd, CH-4002 Basel, Switzerland; Hoffmann La Roche Inc, Nutley, NJ 07110 USA, ou_persistent22              

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Free keywords: motoneuron; microglia; phagocytosis; cell death; alphaX beta2; CD11c/CD18 integrin; cytokine receptor
 Abstract: Neural injury is known to trigger inflammatory changes, including the synthesis of proinflammatory cytokines such as interleukin-1-beta (IL1beta), tumor necrosis factor-alpha (TNFalpha), and interferon-gamma (IFNgamma) [G. Raivich, L. L. Jones, C. U. A. Kloss, A. Werner, H. Neumann, and G. W. Kreutzberg, 1998, J Neurosci, 18: 5804 -5816] that may play a pivotal role in mediating the cellular response in the affected brain tissue. Here we examined the effects of transgenic deletion of receptors for these cytokines on neuronal cell loss in the adult mouse facial motor nucleus after a peripheral, facial nerve cut. Homozygous deletion of IL1 receptor 1 (ILIRl), TNF receptor 1 or 2 (TNFR1 or TNFR2), or IFNgamma receptor 1 (IFNgammaR1) alone had no effect but combined deletion of TNFR1 and TNFR2 caused a striking absence of alphaX beta2 integrin/IBA1-double-labeled, phagocytic microglial nodules in the axotomized facial motor nucleus 14 days after nerve cut. Moreover, this combined deletion also led to an almost complete prevention of cell loss by Day 29. Additional neuronal cell counts at Day 60 revealed a second phase of motoneuron cell disappearance, which did not depend on the presence of TNF receptors. However, there was still the same 22% difference in the total number of motoneurons between the wild-type and TNFR1 & 2-deficient mice, underlining the role of TNF ligands and both TNF receptors in mediating the early phase of neuronal cell loss after traumatic injury. (C) 2002 Elsevier Science (USA).

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Language(s): eng - English
 Dates: 2002-12
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 27071
ISI: 000179988500004
DOI: 10.1006/exnr.2002.8024
 Degree: -

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Title: Experimental Neurology
  Other : Exp. Neurol.
Source Genre: Journal
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Publ. Info: San Diego, CA : Academic Press
Pages: - Volume / Issue: 178 (2) Sequence Number: - Start / End Page: 186 - 193 Identifier: ISSN: 0014-4886
CoNE: https://pure.mpg.de/cone/journals/resource/991042743109584