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Soluble TNFR1 inhibits the development of experimental autoimmune neuritis by modulating blood–nerve-barrier permeability and inflammation
- Source :
-
Journal of Neuroimmunology . Feb2007, Vol. 183 Issue 1/2, p118-124. 7p. - Publication Year :
- 2007
-
Abstract
- Abstract: The role of TNFα/LTα during EAN induced by active immunization with peripheral nerve myelin was examined by administering a recombinant soluble chimeric form of human TNF receptor 1 (TNFR1-IgG). TNFα and LTα do not directly contribute to neurological deficit during EAN since treatment with TNFR1-IgG after onset failed to alter the course of disease. Prophylaxis with a single dose of TNFR1-IgG delayed the onset of EAN and was accompanied initially by inhibition of blood–nerve-barrier permeability and inflammation. Subsequently, the number of infiltrating macrophages and blood–nerve-barrier permeability increased but the disease symptoms remained mild for five days (on average a limp tail) after which severe EAN developed. The antibody titer to peripheral nerve myelin was unaltered by prophylaxis with TNFR1-IgG. The markedly altered tempo of disease onset after TNFR1-IgG prophylaxis indicates that TNFα and/or LTα have a key role in the development of blood–nerve-barrier permeability and the coupling of macrophage activation and recruitment to peripheral nerve pathology during EAN. [Copyright &y& Elsevier]
- Subjects :
- *TUMOR necrosis factors
*NEURITIS
*AUTOIMMUNE diseases
*INFLAMMATION
Subjects
Details
- Language :
- English
- ISSN :
- 01655728
- Volume :
- 183
- Issue :
- 1/2
- Database :
- Academic Search Index
- Journal :
- Journal of Neuroimmunology
- Publication Type :
- Academic Journal
- Accession number :
- 24005644
- Full Text :
- https://doi.org/10.1016/j.jneuroim.2006.11.027