IL-10在过敏性紫癜血管内皮损伤中的作用机制研究

目的　探讨白细胞介素 10 (IL 10 )在过敏性紫癜血管内皮损伤中的作用及机制。方法　建立人脐静脉内皮细胞 (HUVEC)培养模型 ,ELISA法检测过敏性紫癜患儿外周血单个核细胞 (PB MC)活化后培养上清IL 6、IL 1β、TNF α、IL 10等细胞因子的含量 ;AnnexinV/PI双染色法 ,流式细胞仪检测过敏性紫癜患儿PBMC培养上清所诱导的内皮细胞凋亡率。结果　①过敏性紫癜组PBMC体外刺激活化后IL 6、IL 1β、TNF α、IL 10等细胞因子的分泌量均明显高于对照组 (P <0 0 1) ,其培养上清诱导的内皮细胞凋亡率 (34 7± 10 3) %明显高于对照组 (3 6± 0 9) %。②抗IL 6、IL 1β、TNF α单克隆抗体联合阻断可明显降低过敏性紫癜患儿PBMC培养上清诱导的内皮细胞凋亡率 (2 2 6±5 9) % ,而抗IL 10单克隆抗体阻断则明显增加过敏性紫癜患儿PBMC培养上清诱导的内皮细胞凋亡率 (5 6 9± 16 5 ) %。③于过敏性紫癜患儿PBMC培养上清加入外源性IL 10 ,可明显降低IL 6、IL 1β、INF α等炎性细胞因子的表达 ,并明显降低内皮细胞凋亡率 (11 8± 3 1) %。结论　IL 10作为机体炎症反应负反馈调节过程中的一个重要枢纽 ,在过敏性紫癜炎症因子所介导的血管内皮损伤中起重要的保护作用。     

小儿特发性血小板减少性紫癜发病机制的研究

本文采用体外建立抗原—抗体—补体反应体系的试验方法,通过测定该反应体系的血小板~(51)Cr 释放量来进一步探讨特发性血小板减少紫癜(ITP)患儿血小板的破坏机制。结果45例ITP 惠儿其血小板~(51)Cr 释放量与正常值比较明显增高(P<0.01),急慢性之问无显著差异性。45例患儿中有31例血小板~(51)Cr释放量高出正常值上限。同时观察ITP 患儿血清对血小板超微形态和结构的影响,发现血小板表面有圆钝伪足形成,血小板聚集,血小板脱颗粒和空泡性变。正常儿血清对血小板超微形态和结构无明显影响。作者认为,ITP 患儿的血小板相关抗体,能介导血管内血小板的溶解与破坏,其既影响血小板数量,又改变血小板的结构,二者都是导致该病出血的重要原因。     

影像学检查在儿童过敏性紫癜的临床价值

目的探讨儿童过敏性紫癜的影像学特点及其临床价值。方法回顾性分析32例过敏性紫癜并发肠套叠患儿的临床及影像学资料。结果出现并发症之前过敏性紫癜的腹部X线主要表现为局限性小肠充气扩张，粘膜增粗，肠间隙增宽，可伴有液平；B超显示为不同程度的多发节段性肠壁水肿增厚，肠管狭窄等表现；出现并发症后，其X线表现加重，部分病例伴有肠穿孔；B超及X线监视下空气灌肠可以明确是否并发肠套叠，部分病例可通过空气灌肠达到复位治疗的目的。结论影像学检查的重要临床价值在于能与需要手术治疗的其他急腹症相鉴别，同时可以了解其是否并发常见的并发症，为临床确定治疗方案提供可靠的信息。     

BK Virus-Specific Antibodies and BKV DNA in Renal Transplant Recipients with BKV Nephritis

We evaluated twenty renal transplant subjects at various stages of BKV nephritis (BKVN) for BKV-specific IgG and IgM antibodies using ELISA technique and BKV-DNA using PCR. They were divided as early onset (n = 7), stabilizing (n = 3), resolved (n = 8) and late onset (n = 2) BKVN. BKV-specific antibodies and BKV-DNA were simultaneously determined. The mean BKV-specific IgG level in early onset and stabilizing BKVN were 64 and 39 EIA units, and were significantly lower than 138 EIA units seen in resolved BKVN, P = 0.007, P = 0.008. The mean BKV-specific IgM levels in stabilizing BKVN was higher than resolved BKVN (130 vs 51 EIA units), P = 0.006. Mean plasma BKV loads for each group were 955,925, 5642 and 42 copies/mL of plasma, respectively. Prospective study in six BKVN cases revealed mean IgG, IgM levels and BKV-DNA at the time of diagnosis of BKVN as 39, 110 EIA units and 586,758 copies/mL of plasma, respectively. After a mean period of 5.2 months, IgG level increased to 120 EIA units (p = 0.0058) and had no detectable viral copies in circulation. Recovery from BKVN and elimination of BKV is associated with the development of BKV-specific IgG antibodies and this provides insight into the role of humoral immunity to BKV in the pathogenesis of BKVN.     

Immune therapy of lupus: what is on the horizon?

Systemic lupus erythematosus (SLE) is a complex disease whichhas posed a continuing challenge to scientists and cliniciansof diverse areas of specialization. It serves as a model forthe study of the mechanisms of autoimmunity—providingan important basis for the development of novel targeted therapiesin lupus and related conditions. The pathophysiology of SLE stems from the abnormal clearanceof apoptotic cells and/or endothelial activation. Material fromdying cells such as apoptotic blebs that are not efficientlyremoved may act as antigenic stimuli and lead to the developmentof autoantibodies with consequent formation of immune complexesand an inflammatory response in a variety of organ systems [1].This     

关木通引起慢性间质性肾炎7例报告

目的　观察关木通所致慢性肾损伤的临床和病理改变特点。方法　本组 7例中 ,男 5例 ,女 2例。 3例服关木通汤药 ,4例服含关木通成药。分析服用时间、累积总量与肾损害首发症状及症状出现时间、肾功能和肾病理改变的关系。结果　汤药组 :服药时间平均 3 3 3个月 ,累积总量平均 82 9 3 g ,首发症状为乏力 3例 ,夜尿增多 2例 ,平均时间为 8 3个月 ,Cr平均 40 2 μmol/L。肾病理 :3例均为重度寡细胞性肾间质纤维化 ,肾小管广泛萎缩。成药组 :服药时间平均 7 5个月 ,累积总量平均 13 6g ,乏力 3例 ,夜尿增多 1例 ,恶心呕吐、头痛头晕 1例 ,平均18 8个月 ,Cr 3 62 8μmol/L。肾病理为重度寡细胞性间质纤维化和灶状纤维化各 2例 ,肾小管灶状萎缩 3例 ,广泛萎缩 1例。结论　汤药组关木通积累大 ,发病时间早 ,肾病理改变重。提示关木通所致肾损其临床表现、病理改变与服用关木通时间、剂量相关。     

The development of anti-glomerular basement membrane nephritis in two children with Alport's syndrome after renal transplantation: characterization of the antibody target

Two children with Alport's syndrome are described, who developed anti-glomerular basement membrane (GBM) antibody-mediated nephritis after renal transplantation. The reactivity of antibodies in their serum with collagenase-solubilized normal GBM was examined by SDS-PAGE with one- and two-dimensional immunoblotting. The specificity was compared with that of antibodies present in serum from a patient with Goodpasture's syndrome, and a mouse monoclonal antibody (MCA-P1), directed against the Goodpasture antigen. All reacted in a similar way with collagenase-solubilized GBM. Since abnormalities in the composition of the GBM are present in Alport's syndrome, it is proposed that differing antigen composition of GBM in the host compared with the donor kidney, together with transplant rejection, may have provoked the development of post-transplant anti-GBM antibodies.     

肾间质纤维化组织来源成纤维细胞血管紧张素Ⅱ1A受体的表达及其生物学意义

用单侧输尿管梗阻的方法诱导小鼠肾间质纤维化，并从中成功地培养出了成纤维细胞。对成纤维细胞血管紧张素Ⅱ１Ａ（ＡＴ１Ａ）受体的表达与细胞增殖和分泌细胞外基质的关系进行了研究。结果发现，从肾间质纤维化组织中培养出的成纤维细胞，细胞增殖和产生纤维连接蛋白及层粘连蛋白的能力明显高于从正常肾间质中培养的成纤维细胞。在单侧输尿管梗阻小鼠的血浆和肾组织中血管紧张素Ⅱ的活性显著升高。从肾间质纤维化组织中培养出的成纤维细胞，ＡＴ１Ａ受体的表达在蛋白质和分子水平上均有明显增高。表明，在肾间质纤维化过程中肾素－血管紧张素系统被激活，对刺激成纤维细胞增殖和产生细胞外基质起着重要作用。