The TLR7 agonist, imiquimod, increases IFN-beta production and reduces the severity of experimental autoimmune encephalomyelitis.
Publication/Presentation Date
4-15-2010
Abstract
Experimental autoimmune encephalomyelitis (EAE) is a well-characterised model of autoimmune inflammatory demyelination. Toll-like receptors (TLRs) recognise microbial components and initiate innate immune responses. We report in this study that TLR7 stimulation by imiquimod, a synthetic analog of ssRNA, suppresses disease severity in a chronic EAE model. Disease suppression is associated with increased IFN-beta production in spleens of mice treated with imiquimod. In vitro experiments on pDCs, which express high levels of TLR7 and are potent producers of IFN-beta, suggest that an amplification loop involving TLR7 and IFNAR is required for the observed effects.
Volume
221
Issue
1-2
First Page
107
Last Page
111
ISSN
1872-8421
Published In/Presented At
O'Brien, K., Fitzgerald, D., Rostami, A., & Gran, B. (2010). The TLR7 agonist, imiquimod, increases IFN-beta production and reduces the severity of experimental autoimmune encephalomyelitis. Journal of neuroimmunology, 221(1-2), 107–111. https://doi.org/10.1016/j.jneuroim.2010.01.006
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
20138374
Department(s)
Administration and Leadership
Document Type
Article