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初发未用抗精神病药物的精神分裂症患者的β2微球蛋白异常:免疫发病机制的证据

Beta2-microglobulin abnormalities in antipsychotic-naïve schizophrenia: evidence for immune pathogenesis.

作者信息

Chittiprol Seetharamaiah, Venkatasubramanian Ganesan, Neelakantachar Narendran, Allha Naveen, Shetty Kurudunje Taranath, Gangadhar Bangalore N

机构信息

Department of Neurochemistry, National Institute of Mental Health and Neurosciences, Bangalore 560029, India.

出版信息

Brain Behav Immun. 2009 Feb;23(2):189-92. doi: 10.1016/j.bbi.2008.08.007. Epub 2008 Sep 3.

Abstract

Studies examining immune dysfunction in schizophrenia have reported decreased type-1 T-helper cell specific immunity (Th1) and increased type-2 T-helper cell specific immunity (Th2) and related abnormalities in inflammatory system. Beta2-Microglobulin (beta2M) influences the development of dendritic cells, which play a significant role in regulating the differentiation of naive CD4+ T cells into Th1 or Th2 lineages. The present study examined serum beta2M in antipsychotic-naïve schizophrenia patients (n=43) in comparison with age, sex, handedness and socioeconomic status matched healthy controls (n=43). Serum beta2M was significantly higher in schizophrenia patients (1692.6+/-354.4 ng/mL) than healthy controls (1409.6+/-246.9 ng/mL) (t=4.3; p<0.0001). There was a significant positive correlation between beta2M level and total psychopathology score (r=0.32; p=0.035). These novel observations suggest that beta2M abnormalities might have a potential association with the pathogenesis of schizophrenia.

摘要

研究精神分裂症免疫功能障碍的报告显示,1型辅助性T细胞特异性免疫(Th1)降低,2型辅助性T细胞特异性免疫(Th2)增加,且炎症系统存在相关异常。β2微球蛋白(β2M)影响树突状细胞的发育,而树突状细胞在调节初始CD4 + T细胞向Th1或Th2谱系的分化中起重要作用。本研究检测了43例未使用过抗精神病药物的精神分裂症患者的血清β2M,并与年龄、性别、利手和社会经济地位相匹配的43名健康对照者进行比较。精神分裂症患者的血清β2M(1692.6±354.4 ng/mL)显著高于健康对照者(1409.6±246.9 ng/mL)(t = 4.3;p < 0.0001)。β2M水平与总精神病理学评分之间存在显著正相关(r = 0.32;p = 0.035)。这些新发现表明,β2M异常可能与精神分裂症的发病机制存在潜在关联。

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