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目的 研究造模时间及免疫次数对促甲状腺激素受体（TSHR）A亚单位的重组腺病毒（Ad-TSHR289）诱导的毒性弥漫性甲状腺肿（Graves病）模型的影响.方法45只BALB/c小鼠分别注射对照腺病毒（Ad-Lacz）或Ad-TSHR289,于第2次免疫后2周或第3次免疫后4周处死.所有小鼠均采取摘眼球取血,放免法检测血清促甲状腺激素受体抗体（TRAb）以及总甲状腺素（TT4）水平;剥离甲状腺,进行组织学检查.结果 所有注射Ad-TSHR289的小鼠相对于对照组TRAb均明显升高;5周-造模组、10周-造模组的Graves病发病率分别为56%（9/16）、75%（9/12）;10周-造模组甲状腺组织学改变与TT4水平变化吻合度为100%,相对于5周-造模组的50%（8/16）明显升高.结论 10周-造模组相对于5周-造模组具有发病率高、组织学改变与血清TT4水平吻合度高等优势;造模时间以及免疫次数均对该Graves病模型有着较大的影响.

神经系统自身免疫性疾病是以自体免疫细胞、免疫分子等攻击神经系统为主要病理机制的自身免疫性疾病，可发生在中枢神经系统、周围神经系统及神经．肌肉接头处，导致神经元或轴索损伤、髓鞘脱失、神经-肌肉接头破坏等病理改变。在中枢神经系统以多发性硬化（MS）、视神经脊髓炎（NMO）为代表，在周围神经系统以急性炎性脱髓鞘性多发性神经病（AIDP）如格林-巴利综合征（GBS）为代表，

目的 研究蛋白芯片技术对自身抗体检测的敏感性及特异性，探讨其对自身免疫性疾病的鉴别诊断价值，并对其方法学进行评估。方法 用胶体金标法、间接免疫荧光法及蛋白芯片法检测抗ds-DNA；用免疫印迹法、蛋白芯片法检测抗Sm、抗u1RNP、抗SSA、抗SSB、抗Rib-P、抗Jo-1及抗Sol-707种自身抗体，对检测结果进行统计学分析。结果 抗dsDNA抗体检测，蛋白芯片法优于胶体金标法(P<0．01)；皮肌炎和多发性肌炎(DM／PM)组Jo-1抗体(P<0．01)、混合性结缔组织病(MCTD)组u1RNP抗体(P<0．01)、硬皮病(PSS)组gel-70抗体(P<0．05)，蛋白芯片法与免疫印迹法检测结果存在显著性差异；在DM／PM组、PSS组、MCTD组，蛋白芯片法与免疫印迹法对自身免疫性疾病的鉴别诊断有显著性差别(P<0．05)。4种方法的总体敏感性依次为蛋白芯片法、免疫印迹法、间接免疫荧光法、胶体金标法。结论 蛋白芯片法检测项目多、简便快速、敏感性好、特异性强、分析客观，值得推广使用。

目的 探讨辅助性T淋巴细胞亚群Th1／Th2及B细胞在肺炎支原体(MP)下呼吸道感染患儿免疫学发病机制中的作用。方法 应用流式细胞仪单克隆抗体免疫荧光标记法，对30例MP下呼吸道感染患儿的外周血B淋巴细胞CDl9^+及辅助性T淋巴细胞Th1亚群CD4^+CD45RA^+、Th^2亚群CD4^+CD45RO^+的表达情况进行研究。结果 MP下呼吸道感染患儿外周血B淋巴细胞CD19^+表达明显升高。辅助性T淋巴细胞Th1亚群CD4^+CD45RA^+表达明显升高，Th2亚群CD4^+CD45RO^+表达无显著性变化。CD4^+CD45RA^+／CD4^+CD45RO^+明显升高。结论 MP下呼吸道感染患儿存在多种免疫失衡和紊乱情况，主要表现为Th1细胞为主的免疫反应及B淋巴细胞过度增殖，符合自身免疫性疾病的免疫病理基本特征，推测MP下呼吸道感染与自身免疫性疾病密切相关。

目的 探讨自然杀伤T细胞(natural killer T cell,NK T)在Graves''病发病中的作用。方法 用表达有人TSH受体的细胞免疫NKT细胞缺如小鼠和野生型BLAB/c小鼠，每两周一次，共6次。在最后一次免疫结束后两周处死小鼠，检测血清甲状腺素水平，TSH受体抗体。结果 免疫后的NKT细胞缺如小鼠，血清TT4和TRAb水平轻度升高，并且与对照组比较，有显著性差异。但是，在经免疫的NKT细胞缺如小鼠和野生型小鼠之间，血清平均TT4水平和TRAb水平相似，且TSAb与TSBAb水平变化两组之间无显著性差异。结论 NKT细胞可能不参与Graves'病的发生。

目的克隆人促甲状腺激素受体胞外段基因,构建重组真核表达质粒,获得具有免疫学活性的纯化重组蛋白。方法应用RT-PCR技术从人甲状腺组织得到TSHR膜外区cDNA,插入真核表达载体pcDNA3.1（＋）,转染CHO细胞,RT-PCR鉴定基因转录,用免疫细胞化学染色法和Western Blot鉴定表达蛋白。结果经测序证实筛选得到的重组体中存在序列正确的TSHR膜外区基因,表达蛋白具有免疫活性。结论成功克隆了人促甲状腺素受体膜外区基因和构建了真核表达载体,并将其在真核细胞中成功表达。

目的 了解目前陕西地区自身免疫性甲状腺疾病（AITD）患者碘的营养状况，初步探讨人体内碘的代谢状况与AITD发生、发展的关系。方法 收集病例388例，其中AITD患者283例，非AITD对照105例。进行问卷调查，了解研究对象的一般情况；记录甲状腺的大小、形态、质地等情况；测定尿碘浓度、甲状腺功能以及甲状腺自身抗体。应用SPSS12．0进行数据处理。结果 研究人群中Grave’s病（GD）组的尿碘中位数是212μg／L，桥本甲状腺炎（HT）组是245．4μg／L，对照组是197．8μg／L，三组的尿碘分布有统计学差异。HT组患者在不同的尿碘水平上，血清甲状腺球蛋白抗体（TGAb）、甲状腺微粒体抗体（TMAb）以及高敏促甲状腺激素（HS-TSH）水平的差别无统计学差异。结论 在AITD患者中存在饮食碘过多的问题，此可能在AITD的发病中起作用。

The human liver is usually perceived as a non-immunological organ engaged primarily in metabolic, nutrient storage and detoxification activities. However, we now know that the healthy liver is also a site of complex immunological activity mediated by a diverse immune cell repertoire as well as non-hematopoietic cell populations. In the nondiseased liver, metabolic and tissue remodeling functions require elements of inflammation. This inflammation, in combination with regular exposure to dietary and microbial products, creates the potential for excessive immune activation. In this complex microenvironment, the hepatic immune system tolerates harmless molecules while at the same time remaining alert to possible infectious agents, malignant cells or tissue damage. Upon appropriate immune activation to challenge by pathogens or tissue damage, mechanisms to resolve inflammation are essential to maintain liver homeostasis. Failure to clear ＇dangerous＇ stimuli or regulate appropriately activated immune mechanisms leads to pathological inflammation and disrupted tissue homeostasis characterized by the progressive development of fibrosis, cirrhosis and eventual liver failure. Hepatic inflammatory mechanisms therefore have a spectrum of roles in the healthy adult liver; they are essential to maintain tissue and organ homeostasis and, when dysregulated, are key drivers of the liver pathology associated with chronic infection, autoimmunity and malignancy. In this review, we explore the changing perception of inflammation and inflammatory mediators in normal liver homeostasis and propose targeting of liver-specific immune regulation pathways as a therapeutic approach to treat liver disease.

Inflammasomes are multi-protein signaling complexes that trigger the activation of inflammatory caspases and the maturation of interleukin-1β. Among various inflammasome complexes, the NLRP3 inflammasome is best characterized and has been linked with various human autoinflammatory and autoimmune diseases. Thus, the NLRP3 inflammasome may be a promising target for anti-inflammatory therapies. In this review, we summarize the current understanding of the mechanisms by which the NLRP3 inflammasome is activated in the cytosol. We also describe the binding partners of NLRP3 inftammasome complexes activating or inhibiting the inflammasome assembly. Our knowledge of the mechanisms regulating NLRP3 inflammasome signaling and how these influence inflammatory responses offers further insight into potential therapeutic strategies to treat inflammatory diseases associated with dysregulation of the NLRP3 inflammasome,

Over the past decades the notion of ＇inflammation＇ has been extended beyond the original hallmarks of rubor （redness）, calor （heat）, tumor （swelling） and dolor （pain） described by Celsus. We have gained a more detailed understanding of the cellular players and molecular mediators of inflammation which is now being applied and extended to areas of biomedical research such as cancer, obesity, heart disease, metabolism, auto-inflammatory disorders, autoimmunity and infectious diseases. Innate cytokines are often central components of inflammatory responses. Here, we discuss how the type I interferon and interleukin-1 cytokine pathways represent distinct and specialized categories of inflammatory responses and how these key mediators of inflammation counter-regulate each other.