quetiapine, an atypical antipsychotic, is protective against autoimmune-mediated demyelination by inhibiting effector t cell proliferation喹硫平,非典型抗精神病药物,预防谷脱髓鞘通过抑制效应t细胞增殖.pdfVIP
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quetiapine, an atypical antipsychotic, is protective against autoimmune-mediated demyelination by inhibiting effector t cell proliferation喹硫平,非典型抗精神病药物,预防谷脱髓鞘通过抑制效应t细胞增殖
Quetiapine, an Atypical Antipsychotic, Is Protective
against Autoimmune-Mediated Demyelination by
Inhibiting Effector T Cell Proliferation
1. 2. 1 1 1 1 3
Feng Mei , Sheng Guo , Yangtao He , Linyun Wang , Hongkai Wang , Jianqin Niu , Jiming Kong ,
4 2 1
Xinmin Li , Yuzhang Wu , Lan Xiao *
1 Department of Histology and Embryology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China, 2 Department of
Immunology, Third Military Medical University, Chongqing, China, 3 Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Canada,
4 Department of Psychiatry, University of Manitoba, Winnipeg, Canada
Abstract
Quetiapine (Que), a commonly used atypical antipsychotic drug (APD), can prevent myelin from breakdown without
immune attack. Multiple sclerosisis (MS), an autoimmune reactive inflammation demyelinating disease, is triggered by
activated myelin-specific T lymphocytes (T cells). In this study, we investigated the potential efficacy of Que as an immune-
modulating therapeutic agent for experimental autoimmune encephalomyelitis (EAE), a mouse model for MS. Que
treatment was initiated on the onset of MOG35–55 peptide induced EAE mice and the efficacy of Que on modulating the
immune response was determined by Flow Cytometry through analyzing CD4+/CD8+ populations and the proliferation of
effector T cells (CD4+CD252) in peripheral immune organs. Our results show that Que dramatically attenuates the severity of
EAE s
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