弓形体病12例临床分析

报道弓形体病12例，其中，男女各6例，以20－30岁者为多，农民和农村学生占7例。主要症状是发热，乏力，头昏，畏寒，腹胀和纳差；主要体征有肝，脾，淋巴结肿大和下肢出血点。根据临床表现和血清免疫学检查阳性而确诊。以螺旋霉素和复方新诺明联合治疗，7天为一疗程，1－4个疗程后，11例好转或痊愈，1例死亡。有免疫缺陷或免疫务受损者以及胎儿易感染本病。急性感染的后果取决于宿主的免疫状态。     

细胞因子信号转导抑制因子3与早产关系的研究

目的 探讨细胞因子信号转导抑制因子3（SOCS3）与早产的关系.方法 选取2013年2月至2013年10月本院收治自发性早产患者及足月妊娠妇女各30例为研究对象,自发性早产患者为实验组,足月妊娠妇女设为对照组,收集两组胎盘组织,应用RT-PCR及Western-blot检测两组孕妇胎盘组织中的SOCS3蛋白及mRNA的表达情况,比较不同组间SOCS3表达强度;采用RT-PCR检测胎盘组织中IFN-α、IL-10基因表达情况,分析Th1/Th2平衡情况.结果 PCR检测结果显示,SOCS3-mRNA在对照组和实验组胎盘组织中均有表达,对照组SOCS3-mRNA表达强度值明显低于实验组（P ＜0.01）;West-ern-blot结果显示,实验组胎盘组织中SOCS3的蛋白表达明显强于对照组（P＜0.01）,SOCS3基因及蛋白表现一致;实验组患者Th1分泌的细胞因子IFN-α表达显著高于对照组（P＜0.01）,Th2分泌的细胞因子IL-10介导的体液免疫功能减弱（P＜0.05）,Th1/Th2平衡向Th1偏离.结论 早产发生与SOCS3高表达有一定的关系,其作用机制可能是其通过的信号传导及转录活因子（JAK/STAT）信号途径调节体内免疫平衡.为早产研究奠定了基础.     

苦地丁对小鼠免疫功能影响的实验研究

目的　探讨苦地丁对小鼠免疫功能的影响。方法　实验组小鼠灌胃给苦地丁水煎剂 (0 .2g ml) ,每次 0 .5ml,每日 1次 ;对照组小鼠灌胃给同等量生理盐水 ;7d后两组小鼠同时测定脾、胸腺重量 ,腹腔巨噬细胞吞噬功能 ,脾淋巴细胞增殖反应及IL 2活性。结果　苦地丁可使脾和胸腺萎缩 ,巨噬细胞吞噬功能降低 ,淋巴细胞增殖反应受到抑制 ,IL 2活性减弱 ,与对照组比较具有非常显著性差异 (P <0 .0 1)。结论　苦地丁对小鼠免疫功能有明显的抑制作用     

LPSp对狂犬病疫苗佐剂效应及安全性研究

目的研究成团泛菌脂多糖(LPSp)作为狂犬病疫苗佐剂的可行性。方法将Balb/c小鼠32只随机分为空白对照组(注射生理盐水)、LPSp对照组(注射LPSp)、狂犬病病毒蛋白组(注射狂犬病病毒蛋白)、LPSp实验组(注射LPSp和狂犬病病毒蛋白),分别在第0、7、15、21天经背部皮下免疫接种共4次。在免疫接种后第7、14、21、30、45、60天采集小鼠眼内眦静脉血,分离血清,末次采血后处死小鼠。用酶联免疫吸附试验(ELISA)检测血清抗狂犬病病毒IgG,并进行血液学、血液生化、脏器指数等检查。结果免疫接种4次后,LPSp能明显增强狂犬病病毒蛋白免疫小鼠产生IgG的能力(P<0.05);实验期间各组小鼠未发现明显异常表现,体质量、血液学、血液生化和脏器指数等各组间未见明显差异(P>0.05)。结论 LPSp对狂犬病病毒蛋白具有较好佐剂效应;在本实验条件下,LPSp对小鼠安全性好。     

HBV DNA原位杂交与HBsAg免疫金银法双标记技术

用生物素标记HBV DNA探针与免疫金银法相结合,对5例慢性活动性乙型肝炎肝组织进行了原位杂交与免疫组化双染色。结果显示,在同一组织切片上,HBV DNA阳性物(鲜红色)与HBsAg阳性物(黑色)对比鲜明,背景清晰,组织结构完整,方法稳定。文中讨论了影响双染色的几个重要因素。     

调气消积汤对Lewis肺癌小鼠免疫功能影响的实验研究

[目的]探讨调气消积汤对Lewis肺癌小鼠免疫功能的影响。[方法]C57BL/6小鼠常规接种Lewis肺癌,随机分为:荷瘤对照组(MG)、调气消积汤组(TG)、顺铂组(DG)、综合组(ZG);健康的小鼠组成空白对照组(CG),每组10只。观察各组对脾脏指数的影响,计数小鼠外周血T淋巴细胞转化率及脾T淋巴细胞的增殖情况,检测肿瘤坏死因子-α(TNF-α)的表达。[结果]调气消积汤可使荷瘤小鼠的脾脏指数降低并趋向正常,与空白组比较无差异(P>0.05)。从小鼠T淋巴细胞转化率及增殖活性来看,调气消积汤组比荷瘤对照组明显升高,差异显著(P<0.01)。调气消积汤组移植瘤TNF-α蛋白的表达,与荷瘤对照组比较无明显差异(P>0.05)。[结论]调气消积汤对Lewis肺癌小鼠的免疫器官(脾)有一定的保护作用;可以通过提高荷瘤小鼠外周血T淋巴细胞转化率、脾T淋巴细胞增殖活性,来增强荷瘤小鼠的免疫功能;对肿瘤组织中TNF-α蛋白的表达无明显促进和抑制作用。     

Eosinophilic granulomatosis with polyangiitis (Churg–Strauss): state of the art

Eosinophilic granulomatosis with polyangiitis (Churg–Strauss, EGPA) is a systemic small‐vessel vasculitis associated with asthma and eosinophilia. Histology of EGPA shows tissue eosinophilia, necrotizing vasculitis, and eosinophil‐rich granulomatous inflammation. EGPA commonly presents with upper airway tract and lung involvement, peripheral neuropathy, cardiac and skin lesions. Antineutrophil cytoplasmic antibodies (ANCA) are positive in ∼40% of the cases and more often in patients with clinical manifestations due to small‐vessel vasculitis. The pathogenesis of EGPA is multifactorial: the disease can be triggered by exposure to allergens or drugs, but a genetic background has also been recognized, particularly an association with HLA‐DRB4. Th2 responses are prominent, with up‐regulation of IL‐4, IL‐13, and IL‐5; however, Th1 and Th17 responses are not negligible. Eosinophils are activated, have a prolonged lifespan and probably cause tissue damage by releasing their granule proteins; their tissue recruitment can be regulated by chemokines such as eotaxin‐3 and CCL17. Humoral immunity is also dysregulated, as demonstrated by prominent IgG4 and IgE responses. EGPA promptly responds to glucocorticoid therapy, although combinations of glucocorticoids and immunosuppressants (e.g., cyclophosphamide, azathioprine) are eventually required in most cases. Newer therapeutic options include the anti‐IL5 antibody mepolizumab, whose efficacy has been described in small clinical trials, and the B‐cell‐depleting agent rituximab, reported in several case series.     

Regulatory T Cells in Immunologic Self-Tolerance and Autoimmune Disease

Naturally arising CD25⁺CD4⁺ regulatory T cells play key roles in the maintenance of immunologic self-tolerance and negative control of various immune responses. The majority, if not all, of them are produced by the normal thymus as a functionally distinct T-cell subpopulation, and their generation is in part developmentally controlled. Genetic abnormality in the development and function of this population can indeed be a cause of autoimmune disease, immunopathology, and allergy in humans. This regulatory population can be exploited to prevent and treat autoimmune disease by strengthening and reestablishing immunologic self-tolerance.     

Chronic mucocutaneous candidiasis due to gain‐of‐function mutation in STAT1

Chronic mucocutaneous candidiasis (CMC) is a heterogenous group of primary immunodeficiency diseases characterised by susceptibility to chronic or recurrent superficial Candida infection of skin, nails and mucous membranes. Gain‐of‐function mutations in the STAT1 gene (STAT1‐GOF) are the most common genetic aetiology for CMC, and mutation analysis should be considered. These mutations lead to defective responses in Type 1 and Type 17 helper T cells (Th1 and Th17), which, depending on the mutation, also predispose to infection with Staphylococci, Mycobacteria and Herpesviridae. We describe the clinical and genetic findings for three patients with CMC due to gain‐of‐function mutations in the STAT1 gene.