Abstract
BackgroundMultiple sclerosis (MS) is an autoimmune disease causing multifocal demyelination and axonal injuries in the central nervous system (CNS). Toll-interleukin-1 receptor (TIR)-domain containing adaptor protein-inducing interferon beta (TRIF) is an important adaptor protein for Toll-like receptors (TLRs) and can modulate the immune response via regulating cytokine secretion. This study investigated the potential function of TRIF in MS mice via small interference RNA (siRNA).Material/MethodsIsolated mouse lymphocytes were processed using TRIF siRNA, followed by RT-PCR assay to quantify TRIF expression level. An experimental allergic encephalomyelitis (EAE) model was prepared in C57BL/6 mice immunized with MOG 35–55. TRIF siRNA or controlled siRNA were intravenously applied to evaluate the neurological function of animals. Serum levels of IFN-γ and IL-2 were observed.ResultsSpecific siRNA effectively decreased the TRIF expression in mouse dendritic cells and this siRNA improved the EAE severity and neurological scores. Further assays showed that both IFN-γ and IL-2 levels in the siRNA treatment group were significantly lower than in controls.ConclusionsThe expression of TRIF can be down-regulated by siRNA, thereby alleviating the severity of EAE via its inhibition of interleukin and cytokine release. This may provide new insights for future treatment of MS.
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call