学　术

　　人力资源部教师发展中心“学术沙龙”活动特别邀请泰国曼谷朱拉隆功大学Michael H.J.Maes教授来校作学术交流。具体安排如下，欢迎广大师生参加。

　　一、主　题：Schizophrenia and deficit schizophrenia: neuro-immune disorders

　　二、时　间：2019年12月20日（周五）9:00-10:00

　　三、地　点：沙河校区主楼中335会议室

　　四、主讲人：Michael H.J.Maes 教授

　　五、主持人：牟雁东 教授

　　六、主讲人简介：

　　Michael H.J. Maes是一位全球高被引科学家，H-index>120。现任泰国曼谷朱拉隆功大学教授，澳大利亚迪肯大学精神病学荣誉教授；保加利亚普罗夫迪夫医科大学精神病学教授。他在国际期刊上发表了800多篇科学论文，曾在比利时、荷兰、美国、意大利、德国、巴西、澳大利亚、保加利亚和泰国等不同大学担任临床医生和科学家。他的工作涵盖了神经精神疾病中“途径和药物发现过程”的超多学科领域，研究重点是精神疾病的生物标志物和途径，如抑郁症、慢性疲劳综合症、躁郁症和精神分裂症，以及（神经）免疫疾病，包括帕金森病、多发性硬化症、红斑狼疮、中风、类风湿关节炎和阿尔茨海默症。

　　七、内容简介：

　　Here, we propose a new model of schizophrenia, namely the IRS (immune-inflammatory response system) - CIRS (compensatory immune-regulatory system) model. Different phenotypes of schizophrenia are accompanied by signs of activated IRS and CIRS pathways including first-episode psychosis, acute episodes, and treatment-resistant, chronic and deficit schizophrenia. IRS activation is indicated by increased levels of cytokines produced by macrophage M1, T helper (Th)-1 and Th-17 cells, acute-phase proteins, tryptophan catabolites (TRYCATs), complement factors, increased IgA levels to Gram-negative bacteria and oxidative and nitrosative stress. Signs of CIRS activation include activated Th-2 and T regulatory immune subsets, increased levels of cytokine receptors such as soluble interleukin (IL)-2R, s-IL-1 receptor antagonist (sIL-1RA) and soluble tumor necrosis factor receptor sTNF-R2. These CIRS processes are secondary to IRS activation and downregulate the primary IRS thereby dampening the primary IRS. Patients with deficit schizophrenia show pronounced impairments in the CIRS, including lowered natural IgM responses to oxidative specific epitopes and lowered paraoxonase (PON)1 activity. As such, those patients show upregulated IRS responses following infections and other immune challenges.

　　Increased neurotoxic products of M1, Th-1, Th-2 and Th-17 cells (e.g. CCL2, CCL11, IL-1β, IL-6, TNF-α, IL-4, IL-13, IL-17, HMGB1, TRYCATs) may impact neurocognitive functions and schizophrenia symptoms while impairments in innate immune resiliency by lowered natural IgM and PON1 activity together with upregulated gut paracellular pathways may aggravate the effects of the multiple neurotoxic immune compounds. Moreover, increased levels of CCL11, TRYCATs, zonulin, LPS, and HMGB1 may cause damage to the tight junctions of the BBB thereby allowing the entrance of greater amounts of neurotoxic compounds into the brain.

　　As such, schizophrenia and deficit schizophrenia should be conceptualized as neuro-immune disorders characterized by an activated IRS while deficit schizophrenia is additionally characterized by impairments in innate immune system resiliency against immune-inflammatory and nitro-oxidative responses as well as bacterial translocation. 

　　八、主办单位：人力资源部教师发展中心

　　　　承办单位：医学院

　　　　　　　　　　　　　　　　　　　　　　　人力资源部教师发展中心

　　　　　　　　　　　　　　　　　　　　　　　　　2019年12月16日