A hyper-ferritinemia syndrome evolving in recurrent macrophage activation syndrome,as an onset of amyopathic juvenile dermatomyositis: A challenging clinical case in light of the current diagnostic criteria

Juvenile dermatomyositis is an immune-mediated inflammatory multi-system disease involving mainly striated muscles and skin. Typical dermatological features are fundamental to establish the diagnosis, especially whenever the myopathy is very mild or absent, as it occurs in the form called as amyopathic juvenile dermatomyositis. Sometimes, systemic rheumatic diseases can develop a hyperferritinemia syndrome characterized by hemophagocytosis, namely macrophage activation syndrome, which represents a severe and life-threatening complication. Here, we describe a complex clinical history characterized by a hyper-ferritinemia syndrome after infectious mononucleosis, leading to recurrent episodes of macrophage activation syndrome. Finally, the late onset of several skin changes brought to a diagnosis of amyopathic juvenile dermatomyositis.     

Mucosal Vaccination Shapes the Expression of Salivary Antibodies and Establishment of CD8+ T‐Cells

Background: Mucosal vaccination for preventing periodontitis shows promising results. However, various administration routes and adjuvants may have a substantial role in the efficacy of the vaccination. The aim of the study is to compare different modes of mucosal vaccination with whole‐cell Porphyromonas gingivalis and to test the role of various adjuvants as potential modifiers of this process. Methods: Mucosal vaccine was administered through oral or nasal routes to BALB/C mice. The tested adjuvants included Escherichia coli cholera toxin, E. coli labile toxin (LT), and unmethylated CpG dinucleotide (CpG). Control mice were vaccinated subcutaneously. Saliva and serum were collected; anti–P. gingivalis salivary immunoglobulin A (IgA) and serum IgG were quantified. A quantitative enzyme‐linked immunosorbent assay to measure anti–P. gingivalis IgA levels was established. In addition, cells were extracted from head and neck lymph nodes, and the relative CD8⁺ cells were quantified using flow cytometry. Results: All mucosal vaccination modes induced anti–P. gingivalis salivary IgA but not anti–P. gingivalis serum IgG. Subcutaneous vaccination induced both salivary IgA and serum IgG against P. gingivalis. Mucosal vaccination also induced greater establishment of CD8⁺ cells compared to the subcutaneous vaccination. Oral mucosal vaccinations with LT or CpG were the most efficient for salivary IgA expression and CD8 cell establishment in lymph nodes. Conclusions: Oral and nasal mucosal vaccination induced a local host response with little systemic effect. The use of CpG or LT as adjuvants with the oral mucosal vaccination was the most efficient vaccination mode in the present mouse model.     

氟比洛芬酯与吗啡术后镇痛对消化道肿瘤患者淋巴细胞亚群的影响

目的观察氟比洛芬酯与吗啡术后镇痛对消化道肿瘤患者淋巴细胞亚群的影响。方法选择消化道肿瘤手术患者60例,随机均分为三组。术前氟比洛芬酯组(Ⅰ组)、术后氟比洛芬酯组(Ⅱ组)、单纯吗啡组(Ⅲ组),分别于麻醉诱导前即刻(T1)、术后24h(T2)、术后48h(T3)抽取外周静脉血2ml,测定T细胞分化抗原(CD3 )、辅助性T细胞(CD4 )、抑制性T细胞(CD8 )、CD4 /CD8 表达及淋巴细胞(Lcell)总数。结果Lcell总数三组T2时均低于T1时(P<0·01),Ⅲ组T3时与T1时比较仍明显减少(P<0·05),CD4 Ⅲ组T2时明显低于T1时(P<0·05)。CD3 在T2时Ⅲ组与Ⅰ组比明显减少(P<0·05),CD4 在T1时Ⅲ、Ⅱ组与Ⅰ组比明显减少(P<0·05)。结论三组免疫系统在术后均有不同程度的抑制,但使用氟比洛芬酯对免疫系统有明显的保护作用。     

中性粒细胞/淋巴细胞比值与急性缺血性卒中患者脑微出血的相关性

目的 探讨急性缺血性卒中患者中性粒细胞/淋巴细胞比值(neutrophil to lymphocyte ratio, NLR)与脑微出血(cerebral microbleeds, CMBs)的相关性.方法 连续纳入住院的急性缺血性卒中患者.采用梯度回波T2*加权成像评估CMBs及其数量.采用单变量分析比较CMBs组与非CMBs组的基线资料,利用多变量logistic回归分析确定NLR与CMBs的独立相关性.结果 共纳入218例急性缺血性卒中患者,其中66例(30.3%)伴有CMBs.非CMBs组年龄[(64.7 ± 6.6)岁对(66.9 ± 8.6)岁;t=2.052,P=0.041]、高敏C反应蛋白水平[7.0(2.3~13.9)mg/L对8.9(4.0~28.1)mg/L;Z=2.008,P=0.045]和NLR[1.9(1.4~2.9)对2.3(1.7~3.6);Z=2.071,P=0.038]显著低于CMBs组.多变量logistic回归分析显示,NLR(优势比1.276,95%可信区间1.008~1.670;P=0.045)和年龄(优势比1.044,95%可信区间1.002~1.087;P=0.040)是CMBs的独立危险因素.Spearman相关分析显示,NLR与CMBs严重程度呈显著正相关(r=0.210,P=0.007).结论 在急性缺血性卒中患者中,NLR与CMBs及其严重程度相关,提示炎性反应可能参与了CMBs的发生.     

胰岛素对体外培养人淋巴细胞生成Th1/Th2因子平衡的调节作用

目的 探讨胰岛素（Ins）及Ins受体对免疫系统功能的调节作用。了解Ins对体外培养人Th细胞分泌Th1／Th2类细胞因子的影响。方法 用4种Ins浓度的无血清培养基体外培养、激活人外周血淋巴细胞，ELISA法测定其IL-4、IFN了水平。结果A、B组（Ins浓度分别为10、1nmoi／L）的INF-γ水平低于C、D组（Ins浓度分别为0．1、0nmol／L）（P＜0．05）。而IL-4水平4组间比较差异无统计学意义。A、B组的INF-γ/IL-4比值均显著低于C、D组（P〈0．05）。结论 Ins调节体外培养人淋巴细胞的Th1／Th2平衡。     

淋巴细胞转移干扰素抗病毒活性的机理研究

本文研究了人淋巴细胞与羊膜FL细胞之间干扰素介导的抗病毒活性转移的机理。受者FL细胞表达的抗病毒转移活性具有下述特征:1.用放线菌素D抑制FL细胞的RNA合成,能抑制抗病毒活性的表达;2.共同培养中存在的抗2-5_P_3A_3抗体不干扰细胞间抗病毒活性的转移;3.FL细胞膜上干扰素受体用植物血凝素封闭后,不影响抗病毒活性转移的表达。因此,我们认为,淋巴细胞膜上干扰素活化的第二信使分子可能是在细胞之间传递干扰素信息的重要效应物质。     

维生素D与慢性荨麻疹的研究进展

慢性荨麻疹患者的平均维生素D与对照组相比明显偏低,且与病情严重程度及病程存在负相关.尽管尚不明确其中的因果关系,两者间的潜在联系可能与维生素D所起的免疫调节作用有关.有研究表明,维生素D可通过结合维生素D受体影响下游信号通路及核内转录水平,从而对肥大细胞、淋巴细胞以及嗜酸性粒细胞等多种免疫细胞的功能产生调节效应.维生素D可抑制肥大细胞释放活性介质,还可影响T淋巴细胞亚群动态平衡和迁移,引起干扰素γ水平下降和白细胞介素10水平升高等变化,可能是维生素D影响荨麻疹发病的重要机制.同时,临床药物试验显示,补充维生素D对慢性荨麻疹的治疗具有潜在的辅助作用.因此,若能继续明确维生素D与慢性荨麻疹发病的因果关系,从细胞及基因层面研究维生素D对肥大细胞等主要效应细胞的具体影响,将有助于为慢性荨麻疹的诊断和治疗找到新的理论依据.     

间歇低氧大鼠淋巴细胞促进脑血管内皮细胞凋亡的机制

目的 探讨间歇低氧大鼠淋巴细胞促进脑血管内皮细胞内质网应激凋亡作用及机制。方法 取SD雄性大鼠30只,分为正常对照组、间歇低氧组、抗低氧组,每组各10只; 抗低氧组、间歇低氧组建立间歇低氧大鼠模型,并分别于间歇低氧前半小时腹腔注射100 mg/kg超氧阴离子清除剂和等量生理盐水,1次/d,然后间歇低氧干预8 h/d; 正常对照组维持常氧量,干预6周; 各组干预后分离淋巴细胞,测定CD4⁺、CD8⁺ T细胞凋亡率; 取对数期内皮细胞RBE4,与各组分离淋巴细胞共培养,命名为正常对照RBE4组、间歇低氧RBE4组、抗低氧RBE4组; 4 h后测定培养基上清液中超氧化物歧化酶(Superoxide dismutase,SOD)及丙二醛(Malonaldehyde,MDA)水平、内皮细胞凋亡率、内皮细胞中C增强子结合蛋白同源蛋白(Cenhancer binding protein homologous protein,CHOP)、葡萄糖调节蛋白78(Glucose regulatory protein 78,GRP78)、半胱氨酸天冬氨酸蛋白水解酶-3(Cysteine containing aspartate-specific proteases-3,Caspase-3)mRNA及蛋白水平。结果 与正常对照组比较,间歇低氧组、抗低氧组CD4⁺、CD8⁺ T细胞凋亡率降低,且间歇低氧组低于抗低氧组(P<0.05); 与正常对照RBE4组比较,间歇低氧RBE4组、抗低氧RBE4组上清液中SOD水平降低、MDA水平增高、RBE4凋亡率增高、CHOP,Caspase-3 mRNA及蛋白水平升高、GRP78 mRNA及蛋白水平降低(P均<0.05); 与抗低氧RBE4组比较,间歇低氧组SOD水平降低、MDA水平增高、RBE4凋亡率增高、CHOP,Caspase-3 mRNA及蛋白水平升高、GRP78 mRNA及蛋白水平降低(P均<0.05)。结论 间歇低氧大鼠淋巴细胞促进脑血管内皮细胞凋亡可能通过激发内质网应激而发挥作用。     

离体淋巴细胞经低氧及低氧预处理后免疫指标的变化

目的　观察急性低氧及低氧预处理后淋巴细胞 [Ca2 ]i的变化及与淋巴细胞增殖活化的关系。　方法　取正常人外周静脉血 ,用Ficoll Hypaque密度梯度离心法分离淋巴细胞。实验分 3组 :正常对照组、急性低氧组和低氧预处理组。用Fura 2 /AM荧光分光光度法检测 [Ca2 ]i。用ELISA法检测上清液中IgG和IL 2的分泌量。用MTT法检测淋巴细胞增殖率。　结果　急性低氧后淋巴细胞 [Ca2 ]i明显下降 ,与对照组比较差异有非常显著性意义 (P <0 0 1) ,同时淋巴细胞IgG和IL 2的分泌量以及淋巴细胞增殖反应也明显下降 ,与各自的对照组相比差异有非常显著性意义(P <0 0 1) ;低氧预处理后再进行急性低氧时 ,淋巴细胞 [Ca2 ]i、IgG和IL 2的分泌量以及淋巴细胞增殖反应均恢复到与对照组相近的水平 ,且与急性低氧组比较差异有非常显著性意义 (P <0 0 1)。　结论　急性低氧后淋巴细胞免疫功能下降 ,低氧预处理能改善淋巴细胞的免疫功能 ,其中 [Ca2 ]i的适应性变化发挥了重要作用。