Abstract
A role for innate immunity in inflammation of CNS is being increasingly evidenced. This study focused on determining the role of toll-like receptor 4 (TLR4) and phosphorylation of MyD88/IRAK signaling pathway in systemic lupus erythematosus (SLE) pathogenesis. We used mouse models of SLE (BXSB/Yaa mice) and their controls (C57BL/6 mice). TLR4 significantly phosphorylation of MyD88/IRAK activity and enhanced SLE pathogenesis in BXSB/Yaa mice, whereas the small interference RNA-mediated knockdown of TLR4 activity attenuated SLE activity.
Keywords: TLR4; SLE; MyD88; IRAK
Copyright © 2021 by The American Society for BioMedicine and BM-Publisher, Inc.
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How to cite this article
Li G, Zhao W, Finn TB, Martin W, Leung CJ. TLR4-mediated Neuroinflammation in SLE through phosphorylation of MyD88/IRAK signaling pathway. American Journal of BioMedicine 2021;9(1):1-35.
Research Article
1. Abstract
2. Keywords
3. Introduction
4. Results
5. Discussion
6. References