泼尼松联合甲氨喋啶治疗对系统性红斑狼疮患者炎症因子及免疫球蛋白表达水平的影响

[目的]探讨泼尼松联合甲氨喋啶治疗系统性红斑狼疮(SLE)患者对外周血清中的炎症因子白细胞介素-17(IL-17)和白细胞介素-23(IL-23)及免疫球蛋白表达水平的影响.[方法]在本院治疗的74例SLE患者,随机分为两组,各37例.对照组采用醋酸泼尼松治疗,观察组在对照组基础上联合甲氨喋啶治疗,3个月治疗后对患者治...     

联合免疫预防乙型肝炎病毒宫内感染106例临床观察

目的:探讨孕妇主动与被动联合免疫乙型肝炎病毒(HBV)宫内感染的作用和机理。方法:将106例HBsAg( )孕妇分成两组,预防组60例,自孕妇20周起多次注射乙肝疫苗(HBVac)和乙肝免疫球蛋白(HB IG);对照组46例,不用HBVac和HB IG。母婴血清HBsAg、HBeAg和HBs用固相放免法检测,HBV-DNA用有套式PCR检测。结果:预防组新生儿血清HBsAg和HBV-DNA检出率明显低于对照组(3.3%)与26.1,10%与34.8%)均<0.05;预防组新生儿抗-HBs阳性率显著高于对照组(33.3%与8.7%)P<0.05。结论:孕妇于孕期通过HB IG和HBVac免疫,可有效预防HBV宫内感染,其机理可能为胎儿获得被动免疫。     

自身免疫性甲状腺疾病外周血淋巴细胞体外分泌IgG及抑制功能的研究

本实验在体外测定了自身免疫性甲状腺疾病(autoimmune thyroid disease,AITD)患者外周血淋巴细胞培养的上清IgG含量,并根据Concanaralin(ConA)可诱导抑制性T细胞(suppressor T cell,Ts)的原理,检测了ConA诱导Ts对淋巴细胞分泌IgG的抑制率(suppressiverate,SR)。结果表明AITD患者淋巴细胞分泌IgG与正常人无明显差别(P>0.05),而其SR较正常对照显著低下(P<0.05),且SR与Graves病患者血T_3值呈负相关。实验进一步证明甲状腺素在体外并不影响ConA诱导Ts的抑制作用。本研究结果支持本病具有Ts功能的缺陷,且提示这种异常并不是继发于本病,而是本病原发性的免疫表现。     

乙肝大三阳患者肝细胞损伤与6项免疫指标相关性探讨

目的探讨乙型肝炎大三阳患者肝细胞损伤与血清IgM、IgG、IgA、C3、C4及C反应蛋白（CRP）变化的关系。方法选择乙肝大三阳患者80例，根据丙氨酸氨基转移酶（ALT）值（ALT〉200IU／L和〈40IU／L）分为甲、乙两组，各40例，采用速率散射比浊法测定血清IgM、IgG、IgA、C3、C4及CRP。结果甲组血清IgA、IgG、CRP均高于乙组，两组差异具有统计学意义（P〈0．05）；血清IgM、C3、C4两组差异无统计学意义（P〉0．05）。结论血清IgA、IgG、CRP有助于评估肝细胞损伤程度。     

血清克隆性免疫球蛋白检查在慢性淋巴细胞白血病患者中的预后价值

目的 研究血清克隆性免疫球蛋白(Ig)在慢性淋巴细胞白血病(CLL)患者中表达以及与CLL预后指标的相关性,探讨其在CLL患者预后中的意义.方法 全自动电泳仪及扫描仪分析并记录患者血清蛋白电泳和免疫固定电泳结果,定性Ig重链及轻链类型.利用速率散射比浊法定量测定Ig表达水平.结果 101例CLL患者中20例(19.8％)存在克隆性Ig,克隆性IgG、IgM和IgA的检出率分别为13例(12.9％)、7例(6.9％)和1例(1.0％),其中1例(1.0％)患者存在克隆性IgG和IgM双克隆,2例(2.0％)患者共表达轻链κ、λ.在Binet晚期和血清胸苷激酶1(TK1)高水平组,血清克隆性IgG发生率明显高于Binet早期组(P =0.032)和TK1正常水平组(P =0.013).同时发现,Binet晚期组、TK1高水平组和间期荧光原位杂交(FISH) del(11q22.3)阳性组中,血清克隆IgM发生率分别高于Binet早期组(P =0.037)、TK1正常水平组(P =0.017)和FISH del(11q22.3)阴性组(P=0.006).中位随访30(1～ 101)个月,66例患者诊断后接受化疗,统计发现血清克隆性Ig阳性组患者的无治疗生存(TFS)时间(2个月)较阴性组患者(15个月)短(P =0.024),其中血清克隆性IgM阳性组患者的中位TFS时间(1.5个月)较阴性组患者(15个月)短(P=0.013),但Ig和IgM阳性不是独立的预后因素.结论 部分CLL患者血清中存在克隆性Ig,血清克隆性Ig可成为判断CLL患者预后的指标.     

老年慢性阻塞性肺疾病合并糖尿病患者免疫功能变化及临床意义

【目的】研究老年慢性阻塞性肺疾病（COPD）合并糖尿病（DM ）的患者免疫功能变化及临床意义。【方法】65例年龄大于65岁的老年COPD稳定期患者分为COPD合并DM 组（35例）和COPD组（30例）,同时选择20例健康老年人作为对照组,分别测定外周血细胞免疫和体液免疫指标。【结果】COPD＋ DM 组 IgA、IgG、IgM、CD4＋水平均低于COPD 组和对照组,CD8＋水平高于COPD组和对照组,CD4＋／CD8＋倒置更为明显,差异均有统计学意义（ P ＜0．05）,而CD3＋水平COPD组和COPD＋DM组之间无显著性差异（ P ＞0．05）。【结论】老年COPD合并DM的患者免疫功能低下,预防和控制DM对于提高COPD患者的免疫功能有重要意义。     

蛋白转导结构域介导乙型肝炎病毒聚合酶末端蛋白重链可变区抗体体外抑制病毒的复制

目的 蛋白转导结构域(TAT)介导HBV聚合酶末端蛋白(TP)重链可变区(VH)抗体,研究特异性TAT-VH抗体体外对HBV复制的影响.方法 将TAT-VH基因克隆入原核表达载体pET28a(+),在大肠埃希菌BL21(DE3)LysS内诱导融合蛋白表达并进行纯化.纯化的TAT-VH加入培养的HepG2.2.15细胞,间接免疫荧光法检测其导入HepG2.2.15细胞的效率,四甲基偶氮唑盐(MTT)法检测其对细胞生长代谢的影响,将TAT-VH加入培养的HepG2.2.15细胞,定量PCR法检测HBV DNA水平.数据行单因素方差分析和t检验.结果 成功制备了TAT-VH融合蛋白,间接免疫荧光及MTT证实TAT-VH可以跨膜导入HepG2.2.15细胞,且对细胞生长无影响;加入5 000 nmol/L TAT-VH的HepG2.2.15细胞培养上清液内HBV DNA为(1.211±0.132)lg拷贝/mL,对照组为(5.325±0.041)lg拷贝/mL(t=72.91,P＜0.05);细胞内分别为(3.521±0.411)和(8.532±0.132)Ig拷贝/mL(t=28.41,P＜0.05).结论 HBV聚合酶TP区特异性TAT-VH抗体在体外可抑制HBV复制,为应用细胞内抗体治疗HBV感染提供了良好的实验基础.     

特异性IgY抗体对人牙菌斑中变形链球菌的影响

目的:研究抗变形链球菌葡糖基转移酶过表达株IgY抗体对人牙菌斑中变形链球菌的影响。方法:采用双盲法,选择自愿受试者41名,分为对照组和试验组两组。分别给予含抗变形链球菌葡糖基转移酶过表达株IgY抗体和非特异性IgY抗体的喷雾剂,每日两次,共4周。试验前、试验后1周、试验后4周分别取口腔内指定牙位的菌斑样本,在厌氧的环境中培养,检测变形链球菌菌落数及总厌氧菌菌落数,并计算变形链球菌占总厌氧菌的百分率。结果:使用抗变形链球菌葡糖基转移酶过表达株IgY抗体1周及4周变形链球菌计数较试验前有显著性减少,变形链球菌占总厌氧菌的百分率分别降低12.99%和12.70%,而对照组中的变形链球菌计数和变形链球菌占总厌氧菌的百分率试验前后无显著性差异。结论:抗变形链球菌葡糖基转移酶过表达株IgY抗体可明显减少人牙菌斑中的变形链球菌,改变人牙菌斑的微生物组成,可为防龋提供新的思路。     

Binding of LBP‐1a to specific immunoglobulin switch regions in vivo correlates with specific repression of class switch recombination

Upon stimulation of mature B cells, class switch recombination (CSR) can alter the specific immunoglobulin heavy chain constant region that is expressed. In a tissue culture cell line, we previously demonstrated that inhibition of late SV40 factor (LSF) family members enhanced IgM to IgA CSR. Here, isotype specificity of CSR regulation by LSF family members is addressed in primary mouse splenic B cells. First, we demonstrate that leader‐binding protein‐1a (LBP‐1a) is the prevalent family member in B lymphocytes. Second, we demonstrate by ChIP that LBP‐1a binds genomic sequences around mouse switch (S) regions in an isotype‐specific manner, in accordance with computational predictions: binding is observed to Sμ and Sα, but not to the tested Sγ1, regions. Importantly, binding of LBP‐1a is tightly regulated, with occupancy at genomic S regions dramatically decreasing following LPS stimulation. Finally, the consequence of DNA‐binding by LBP‐1a is determined using bone marrow chimeric mice in which LSF/LBP‐1 activity is inhibited in hematopoietic lineages. Upon in vitro stimulation of such primary B cells, CSR occurs with a higher efficiency to IgA, but not to IgG1. These results are supportive of a model whereby LBP‐1a represses CSR in an isotype‐specific manner via direct interaction with S regions involved in the recombination.     

TT Virus Infection in Patients with Primary Hypogammaglobulinaemia: Natural History and Relationship to Liver Disease in the Immunocompromised Host

Background: TT virus (TTV) is a recently discovered human DNA virus with worldwide distribution, but with no clear disease association. The possibility of an enhanced TTV virulence in patients with immunodeficiencies has not yet been investigated but is of particular interest because other viruses have been demonstrated to cause severe and rapid liver disease in such patients. Here we analysed the characteristics of TTV infection in a large cohort of patients with primary hypogammaglobulinaemia (PHG) and whether TTV has a role in the frequently observed cryptogenic liver disease in these patients. Methods: 83 Norwegian patients with PHG (serum immunoglobulin G _&lt; 2 g/L), receiving substitution treatment with immunoglobulins, were followed regularly for median 10.2 years (range 2-30). TTV DNA was sought in serum samples and three immunoglobulin preparations by polymerase chain reaction; TTV DNA quantitation, DNA sequencing and phylogenetic analysis were performed in selected samples. Results: TTV DNA was detected in 27 of 83 (32.5%) patients and was not associated with a particular type of PHG. The prevalence of TTV infection was dependent on intravenous immunoglobulin administration, duration of therapy and patient's age. TTV DNA was found in two of three currently used immunoglobulin preparations. In the longitudinal study, whether TTV was cleared or newly acquired had no impact on liver function tests and no particular TTV strain was found in patients with more severe liver disease. Conclusions: TTV infection is common in patients with PHG. Treatment with immunoglobulins has a role in the transmission of TTV in these patients. However, we found no evidence of TTV-induced liver disease in this group of immunocompromised patients.