Article
Role for MyD88, TLR2 and TLR9 but not TLR1, TLR4 or TLR6 in experimental autoimmune encephalomyelitis.
Journal of immunology (Baltimore, Md. : 1950) - 15 Jul 2011
Miranda-Hernandez Socorro, Gerlach Nicole, Fletcher Julie M, Biros Erik, Mack Matthias, Körner Heinrich, Baxter Alan G
Abstract excerpt
The potential roles of TLRs in the cause and pathogenesis of autoimmune CNS inflammation remain contentious. In this study, we examined the effects of targeted deletions of TLR1, TLR2, TLR4, TLR6, TLR9, and MyD88 on the induction of myelin oligodendrocyte glycoprotein 35-55 (MOG(35-55)) peptide/CFA/pertussis toxin-induced autoimmune encephalomyelitis. Although C57BL/6.Tlr1(-/-), C57BL/6.Tlr4(-/-) and...
Topics
- Animals
- Cell Movement
- Cells, Cultured
- Encephalomyelitis, Autoimmune, Experimental
- Female
- Gene Silencing
- Genetic Predisposition to Disease
- Glycoproteins
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Myelin-Oligodendrocyte Glycoprotein