The TLR7 agonist, imiquimod, increases IFN-β production and reduces the severity of experimental autoimmune encephalomyelitis

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-β 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-β, suggest that an amplification loop involving TLR7 and IFNAR is required for the observed effects.

Keywords: Toll-like receptors, Autoimmune disease, Experimental autoimmune encephalomyelitis, Multiple sclerosis, Plasmacytoid dendritic cells