Cutting edge: TLR3 stimulation suppresses experimental autoimmune encephalomyelitis by inducing endogenous IFN-β

Tarik Touil, Denise Fitzgerald, Guang Xian Zhang, Abdolmohamad Rostami, Bruno Gran*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

110 Citations (Scopus)

Abstract

Experimental autoimmune encephalomyelitis is a well-characterized model of cell-mediated autoimmunity. TLRs expressed on APCs recognize microbial components and induce innate immune responses, leading to the elimination of invading infectious agents. Certain TLR agonists have been reported to have adjuvant properties in CNS autoimmune inflammatory demyelination. We report in this study that TLR3 stimulation by polyinosinic-polycytidylic acid, a double-stranded RNA analog, suppresses relapsing demyelination in a murine experimental autoimmune encephalomyelitis model. Disease suppression is associated with the induction of endogenous IFN-β and the peripheral induction of the CC chemokine CCL2. These data indicate that a preferential activation of the MyD88-independent, type I IFN-inducing TLR pathway has immunoregulatory potential in this organ-specific autoimmune disease.

Original languageEnglish
Pages (from-to)7505-7509
Number of pages5
JournalJournal of Immunology
Volume177
Issue number11
Publication statusPublished - 01 Dec 2006
Externally publishedYes

ASJC Scopus subject areas

  • Immunology

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