Cutting Edge: TLR3 stimulation suppresses experimental autoimmune encephalomyelitis by inducing endogenous IFN-beta.
Publication/Presentation Date
12-1-2006
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-beta 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.
Volume
177
Issue
11
First Page
7505
Last Page
7509
ISSN
0022-1767
Published In/Presented At
Touil, T., Fitzgerald, D., Zhang, G. X., Rostami, A., & Gran, B. (2006). Cutting Edge: TLR3 stimulation suppresses experimental autoimmune encephalomyelitis by inducing endogenous IFN-beta. Journal of immunology (Baltimore, Md. : 1950), 177(11), 7505–7509. https://doi.org/10.4049/jimmunol.177.11.7505
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
17114417
Department(s)
Administration and Leadership
Document Type
Article