流感疫苗诱导Hela细胞凋亡与免疫调节效应

目的观察流感疫苗诱导Hela细胞凋亡与免疫调节效应。方法将流感疫苗作用于Hela细胞,采用MTT比色法和流式细胞仪检测疫苗对Hela细胞增殖、凋亡和细胞周期的影响;同时用MTT法检测疫苗对小鼠脾细胞增殖的影响;采用结晶紫、中性红染色及MTT法,分别检测脾细胞诱导上清中IFN-γ、IL-2和TNF-α的分泌情况。结果一定浓度流感疫苗能够抑制Hela细胞增殖,促进细胞凋亡,凋亡率可达58·37%;还可促进小鼠脾细胞增殖及Th1型细胞分泌IFN-γ。结论流感疫苗能够抑制Hela细胞增殖,此作用可能是通过诱导Hela细胞凋亡、调节免疫细胞增殖及IFN-γ的分泌而实现的。     

转化生长因子-β在骨髓间充质干细胞治疗实验性自身免疫性重症肌无力机制中的作用

目的探讨转化生长因子-β(TGF-β)在骨髓间充质干细胞(BMSCs)治疗实验性自身免疫性重症肌无力(EAMG)机制中的作用。方法分离培养健康Lewis大鼠BMSCs,并进行大量体外扩增;以大鼠来源的乙酰胆碱受体(R-AChR)2次免疫Lewis大鼠,建立EAMG模型;第2次免疫的同时,经尾静脉移植BMSCs,1×107个/只,依据Lennon评分标准,进行体重测量和临床体征评定。并通过体外实验进一步探讨TGF-β在治疗EAMG过程中的具体机制。结果BMSCs移植明显缓解了EAMG的临床症状,临床评分及体重变化差异均有统计学意义,表明治疗有效;体外实验结果显示,BMSCs能通过TGF-β的分泌影响AChR特异性Th17/Treg细胞亚群的分布及其相关因子的分泌,以anti-TGF-β抗体封闭后,这种调节作用在一定程度上被抑制。结论BMSCs通过细胞因子TGF-β,能在一定程度上调节AChR特异性Th17/Treg细胞亚群的平衡,从而起到治疗EAMG的作用。     

静脉滴注丙种球蛋白治疗病毒性脑炎的临床研究

应用静注丙种球蛋白（IVIg）治疗病毒性脑炎（病脑），同时应用血浆治疗作为对照，观察结果表明症状、体征和实验室检测结果，观察组疗效均明显优于对照组。提示IVIg治疗病脑好转快，疗效好，病死率低，后遗症少。     

重症肌无力患儿免疫状态及静注免疫球蛋白的疗效

目的观察重症肌无力（ＭＧ）患儿机体免疫状态,比较静脉注射免疫球蛋白（ＩＶＩｇ）与免疫调节疗法 对ＭＧ的疗效。方法对８３例ＭＧ患儿分别于治疗前和缓解后,采用单项免疫扩散法检测血清免疫球蛋白（Ｉｇ）,用 ＥＩＪＳＡ法检测乙酸胆碱受体抗体（ＡｃｈＲａｂ）和可溶性白细胞介素－２受体（ＳＩＬ－２Ｒ）,以２４名健康儿童为对照组;并 对上述患儿中的６８例采用免疫调节疗法,２５例采用ＩＶＩｇ疗法。结果初发和复发的ＭＧ患儿ＩｇＧ、ＡｃｈＲａｂ、ＳＩＬ－２Ｒ 明显高于对照组（Ｐ＜０．００１）,缓解后与对照组差异无显著意义（Ｐ＞０．０５）;ＩＶＩｇ治疗组和免疫调节治组疗缓解率均 为９２％,复发率ＩＶＩｇ组为８％,免疫调节组为１８％,两组比较差异有显著意义（Ｐ＜０．０５）。结论ＩｇＧ、ＡｃｈＲａｂ、ＳＩＬ－ ２Ｒ随ＭＧ的病情而变化,可作为预测ＭＧ病情的依据;ＩＶＩｇ疗法在降低复发率方面优于免疫调节疗法。     

免疫调节优化算法及其对控制系统的参数估计

借鉴免疫系统中T细胞调节的思想、抗体重复变异的亲和成熟特征、小生境共享适应度方法及相关的免疫机制,提出一种适合于函数优化的新型智能优化算法。算法设计的关键在于利用T细胞调节机制动态调节参与变异的抗体数日,以及利用抗体亲和成熟特征设计自适应突变的算子模块;突出的优点为自适应能力强、寻优速度快、多途径产生进化群体及易于与相关算法融合。事例仿真效果论证了其可行性和有效性。     

草珊瑚多糖对经脂多糖刺激的RAW264.7巨噬细胞的免疫调节作用研究

为研究草珊瑚多糖对RAW264.7巨噬细胞的免疫调节作用,建立LPS刺激的RAW264.7细胞模型,通过MTT法测定,观察草珊瑚多糖对RAW264.7细胞增殖影响并评价细胞毒性。同时,对草珊瑚多糖抑制模型细胞炎症因子一氧化氮(NO)表达及吞噬活性进行研究。结果表明,草珊瑚多糖可显著抑制RAW264.7细胞增殖水平,其细胞毒性分级为1级或以下。同时,草珊瑚多糖可显著抑制模型细胞NO表达及巨噬细胞吞噬活性。此研究将为深入研究草珊瑚抗炎活性作用机制及草珊瑚资源开发提供理论依据。     

Unraveling the Immune Microenvironment of Thymic Epithelial Tumors: Implications for Autoimmunity and Treatment

Thymic Epithelial Tumors (TETs) represent a rare tumor family, originating from the epithelial component of the thymus gland. Clinicopathologically, they are segregated into six major subtypes, associated with distinct histological features and clinical outcomes. Their emergence and evolution are accompanied by the generation of a complex tumor microenvironment (TME), dominated by phenotypically and functionally divergent immune cellular subsets, in different maturation states and in analogies that vary significantly among different subtypes. These heterogenous leukocyte populations exert either immune-permissive and tumor-suppressive functions or vice versa, and the dynamic equilibrium established among them either dictates the tumor immune milieu towards an immune-tolerance state or enables the development of a productive spontaneous tumoricidal response. The immunologically “hot” microenvironment, defining a significant proportion of TETs, makes them a promising candidate for the implementation of immune checkpoint inhibitors (ICIs). A number of phase I and II clinical trials have already demonstrated significant, type-specific clinical efficacy of PD-L1 inhibitors, even though substantial limitations in their utilization derive from their immune-mediated adverse effects. Moreover, the completed clinical studies involved relatively restricted patient samples and an expansion in the enrolled cohorts is required, so that more trustworthy conclusions regarding the benefit from ICIs in TETs can be extracted.     

维生素A对小鼠免疫调节功能的影响

目的探讨维生素A对小鼠免疫调节功能的影响。方法人工制备低维生素A、正常维生素A、高维生素A3种饲料,分别按常规饲养3组小鼠5周,应用微量荧光法测定血清维生素A浓度,三色流式细胞术测定CD4+T细胞内细胞因子IL-4和IFN-γ水平。结果3组小鼠血清维生素A浓度差异有显著意义,低维生素A组IFN-γ水平(28.60%±10.82%)明显高于正常对照组(20.13%±6.39%);高维生素A组IL-4水平(5.31%±2.04%)明显高于正常对照组(2.80%±1.37%),差异有非常显著意义(均P<0.01)。随着维生素A水平的提高,IFN-γ表达率降低,Th1免疫应答减弱,IL-4表达率增高,Th2免疫应答增强。结论维生素A对小鼠Th1/Th2免疫应答影响显著。     

FoxO3a基因缺失致小鼠脾脏进行性慢性炎性反应的观察

目的观察FoxO3a基因缺失致小鼠脾脏进行性慢性炎性反应。方法分别于16周、24周和12个月称取FoxO3a基因敲除小鼠和对照小鼠体重;于16、24和38周处死各组小鼠,取脾脏,肉眼观察脾脏变化,并制备脾细胞悬液,进行细胞计数,同时取各组小鼠卵巢、肺及皮下等组织,观察其炎性变化。流式细胞术检测24周的FoxO3a基因敲除小鼠和对照小鼠脾细胞中T、B淋巴细胞和Mac-1+细胞数量及百分率;Real-time PCR检测脾细胞中炎性细胞因子S100A8和S100A9基因mRNA的表达水平。结果与对照小鼠相比,FoxO3a基因敲除小鼠脾脏明显肥大,且随年龄增加更加显著,卵巢、肺及皮下等组织内可见大量炎性细胞浸润,脾细胞数明显升高;基因敲除组老年小鼠的体重明显低于对照小鼠;FoxO3a基因敲除小鼠的脾细胞中T、B淋巴细胞数增加明显,但所占脾细胞的百分率无明显增加,Mac-1+细胞数和百分率均明显增加;S100A8和S100A9基因mRNA的表达水平明显高于对照小鼠。结论 FoxO3a基因缺失致小鼠脾脏进行性慢性炎性反应。     

A Review on the Role of Non-Coding RNAs in the Pathogenesis of Myasthenia Gravis

Myasthenia gravis (MG) is an autoimmune condition related to autoantibodies against certain proteins in the postsynaptic membranes in the neuromuscular junction. This disorder has a multifactorial inheritance. The connection between environmental and genetic factors can be established by epigenetic factors, such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). XLOC_003810, SNHG16, IFNG-AS1, and MALAT-1 are among the lncRNAs with a possible role in the pathoetiology of MG. Moreover, miR-150-5p, miR-155, miR-146a-5p, miR-20b, miR-21-5p, miR-126, let-7a-5p, and let-7f-5p are among miRNAs whose roles in the pathogenesis of MG has been assessed. In the current review, we summarize the impact of miRNAs and lncRNAs in the development or progression of MG.