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Rui-Sheng Duan

Researcher at Shandong University

Publications -  33
Citations -  577

Rui-Sheng Duan is an academic researcher from Shandong University. The author has contributed to research in topics: Myasthenia gravis & Immune system. The author has an hindex of 13, co-authored 32 publications receiving 429 citations.

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Atorvastatin ameliorates experimental autoimmune neuritis by decreased Th1/Th17 cytokines and up-regulated T regulatory cells.

TL;DR: There is strong evidence that atorvastatin can act as an inhibitor in EAN by inhibiting the immune response of Th1 and Th17, decreasing the expression of co-stimulatory molecule, and up-regulating the number of T regulatory cells.
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Enhanced glycolysis contributes to the pathogenesis of experimental autoimmune neuritis.

TL;DR: The effects of glycolysis inhibition on both innate and adaptive immune responses and the alleviation of animal clinical symptoms indicated that enhanced gly colysis contributed to the pathogenesis of EAN.
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Exosomes derived from atorvastatin-modified bone marrow dendritic cells ameliorate experimental autoimmune myasthenia gravis by up-regulated levels of IDO/Treg and partly dependent on FasL/Fas pathway

TL;DR: The data suggest that atorvastatin-induced immature BMDCs are able to secrete tolerogenic Dex, which is involved in the suppression of immune responses in EAMG rats, and provides a novel cell-free approach for the treatment of autoimmune diseases.
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M1 Macrophage Derived Exosomes Aggravate Experimental Autoimmune Neuritis via Modulating Th1 Response

TL;DR: A previously undescribed means that M1 macrophages amplify Th1 response via exosomes is identified and novel insights into the crosstalk between macrophage and T cells as well are provided.
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Atorvastatin-modified dendritic cells in vitro ameliorate experimental autoimmune myasthenia gravis by up-regulated Treg cells and shifted Th1/Th17 to Th2 cytokines

TL;DR: This study found that spleen-derived dendritic cells from the ongoing experimental autoimmune myasthenia gravis (EAMG) rats can be induced into tolerogenic DCs by atorvastatin in vitro, and played their immunomodulatory effects in vivo mainly by decreased expression of CD86 and MHC class II on endogenous DCs.