Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 221, Issue 1-2, Pages 107-111Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2010.01.006
Keywords
Toll-like receptors; Autoimmune disease; Experimental autoimmune encephalomyelitis; Multiple sclerosis; Plasmacytoid dendritic cells
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Funding
- Marie Curie International Reintegration Grant
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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. (C) 2010 Elsevier B.V. All rights reserved.
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