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  Lymphocyte infiltration in the injured brain: Role of proinflammatory cytokines

Raivich, G., Bohatschek, M., Werner, A., Jones, L. L., Galiano, M., Kloss, C. U. A., et al. (2003). Lymphocyte infiltration in the injured brain: Role of proinflammatory cytokines. Journal of Neuroscience Research, 72(6), 726-733. doi:10.1002/jnr.10621.

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 Creators:
Raivich, G.1, Author           
Bohatschek, M.1, Author           
Werner, A.1, Author           
Jones, L. L.1, Author           
Galiano, M.1, Author           
Kloss, C. U. A.1, Author           
Zhu, X. Z.2, Author
Pfeffer, K.2, Author
Liu, Z. Q.1, Author           
Affiliations:
1Emeritus Group: Neuromorphology / Kreutzberg, MPI of Neurobiology, Max Planck Society, ou_1113551              
2Univ Coll London, Dept Obstet & Gynaecol, Perinatal Brain Repair Grp, London WC1E 6HX, England.; Univ Coll London, Dept Anat, London WC1E 6HX, England.; Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 200031, Peoples R China.; Tech Univ Munich, Inst Med Microbiol Immunol & Hyg, D-8000 Munich, Germany., ou_persistent22              

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 Abstract: Studies using mouse axotomised facial motoneuron model show a strong and highly selective entry of CD3+ lymphocytes into the affected nucleus, with a maximum at Day 14, which coincides with the peak of neuronal cell death, microglial phagocytosis, and increased synthesis of interleukin-1 beta (IL1beta), tumour necrosis factor-alpha (TNFalpha) and interferon-gamma (IFNgamma) We explored the possible involvement of these cytokines during the main phase of lymphocyte recruitment into the axotomised facial motor nucleus 7-21 days after nerve cut using mice homozygously deficient for IL1 receptor type 1 (IL1R1(-/-)), TNF receptor type 1 (TNFR1(-/-)), type 2 (TNFR2(-/-)) and type 1 and 2 (TNFR1&2(-/-)), IFNgamma receptor type 1 (IFNgammaR1(-/-)), and the appropriate controls for the genetic background. Transgenic deletion of IL1R1 led to a 54% decrease and that of TNFR2 to a 44% reduction in the number of CD3+ T-cells in the axotomised facial motor nucleus, with a similar relative decrease at Day 7, 14, and 21. Deletion of TNFR1 or IFNgammaR1 had no significant effect. Deletion of both TNFR1 and 2 (TNFR1&2(-/-)) caused a somewhat stronger, 63% decrease than did TNFR2 deletion alone, but this could be due to an almost complete inhibition of neuronal cell death. No mutations seemed to inhibit aggregation of CD3+ T-cells around glial nodules consisting of Ca-ion binding adaptor protein-1 (IBA1)+ phagocytotic microglia and neuronal debris. Altogether, the current data show the importance of IL1R1 and TNFR2 as the key players during the main phase of lymphocyte recruitment to the damaged part of the central nervous system. (C) 2003 Wiley-Liss, Inc.

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Language(s): eng - English
 Dates: 2003-06-15
 Publication Status: Published in print
 Pages: -
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 127683
ISI: 000183381000008
DOI: 10.1002/jnr.10621
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Title: Journal of Neuroscience Research
  Alternative Title : J. Neurosci. Res.
Source Genre: Journal
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Pages: - Volume / Issue: 72 (6) Sequence Number: - Start / End Page: 726 - 733 Identifier: ISSN: 0360-4012