Soluble TNFR1 inhibits the development of experimental autoimmune neuritis by modulating blood-nerve-barrier permeability and inflammation

Jude Matthew Taylor, John David Pollard

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)118-124
Number of pages7
JournalJournal of Neuroimmunology
Volume183
Issue number1-2
DOIs
Publication statusPublished - 1 Feb 2007
Externally publishedYes

Keywords

  • Blood-nerve-barrier
  • Demyelination
  • EAN
  • Lymphotoxin
  • Macrophage
  • TNF

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