CD34在IgA肾病肾小管间质病变中的表达及意义

目的:研究白细胞分化抗原CD34在IgA肾病肾小管间质病变中的表达变化,探讨其在IgA肾病进展过程中的作用.方法:应用免疫组织化学双标记技术检测不同小管间质病变程度的IgA肾病患者肾组织内CD34和α-平滑肌激动蛋白(α-SMA)的表达.肾小管间质病变分级采用Katafuchi积分.详细收集每例患者肾活检时的24 h尿蛋白定量(TUPr)及内生肌酐清除率(Ccr),并与免疫病理结果进行相关分析.结果:无小管间质病变组未见CD34的表达,α-SMA仅表达于间质的动脉壁;轻度小管间质病变组CD34和α-SMA表达散在,主要见于小管间质受损部位;中、重度病变组较轻度病变组CD34和α-SMA的表达显著增加(P＜0.05);小管间质内CD34的表达与α-SMA的表达及TUPr、Ccr具有显著相关性(P＜0.05).结论:随小管间质病变进展而出现的CD34表达增多可能在IgA肾病中发挥重要作用.     

CD146在IgA肾病肾小管的表达及临床意义

肾小管问质纤维化是各种肾脏疾病发展至肾衰竭的主要机制.黏附分子在这一过程中起了重要作用.CD146是近年新发现的一种免疫球蛋白超家族类黏附分子,其在肾脏疾病中的作用逐渐引起重视.IgA肾病是导致我国终末期肾病的常见原因.     

CD71与IgA肾病发病机制的探讨

CD71,又称转铁蛋白受体 ,近来发现它在IgA肾病系膜细胞上高表达 ,而且是IgA的受体 ,在IgA沉积中可能起着关键的作用 ,因此对CD71的表达、功能和与肾病关系的探讨有助于对IgA肾病发病机制的进一步理解 ,而且给IgA肾病的诊断提供另一有力的证据 ,对IgA肾病的治疗提供一新的途径。     

CD71与IgA肾病发病机制的探讨

CD71，又称转铁蛋白受体，近来发现它在IgA肾病系膜细胞上高表达，而且是IgA的受体，在IgA沉积中可能起着关键的作用，因此对CD71的表达、功能和与肾病关系的探讨有助于对IgA肾病发病机制的进一步理解，而且给IgA肾病的诊断提供另一有力的证据，对IgA肾病的治疗提供一新的途径。     

活化白细胞黏附分子在IgA肾病中的表达及意义

目的:探讨活化白细胞黏附分子(CD166)在IgA肾病中的表达及与IgA肾病临床病理特征的关系.方法:用免疫组化二步法检测CD166蛋白在79例IgA肾病患者肾组织的表达.结果:CD166在IgA肾病患者肾小管、间质普遍表达,按Lee分级的级别增加逐渐增高.与单纯性血尿患者(A组)相比,混合蛋白尿、血尿患者(B组)肾小管间质CD166表达明显增高.肾小管间质CD166表达与患者病理分级、小管间质病变、单个核细胞浸润程度及血清C反应蛋白(CRP)水平正相关.结论:CD166在IgA肾病中表达异常,在IgA肾病小管、间质病变及疾病进展中起一定作用.     

肾平颗粒对IgA肾病小鼠肾组织CD44的影响

目的：探讨肾平颗粒治疗实验性IgA肾病的作用机制。方法：采用口服牛血清白蛋白（Ⅸ讽）及尾静脉注射葡萄球菌肠毒素B（SEB）免疫复合法诱发小鼠IgA肾病模型，随机分为正常组、模型组、洛汀新组及肾平颗粒低、中、高剂量组，共6组。观察治疗前后IgA免疫复合物在肾组织中的沉积，通过免疫组化法检测CD44在肾组织的表达。结果：正常组无IgA沉积，模型组肾小球均出现IgA沉积，而治疗组IgA在肾小球的沉积较模型组明显降低（P〈0．01），正常组仅有少量CD44表达，模型组中CD44的表达明显增强，治疗组（除肾平低剂量组）CD44在肾小球的表达明显减少，并且在肾平颗粒各治疗组中呈剂量依赖关系（P〈0．01）。结论：肾平颗粒能降低IgA肾病小鼠肾组织CD44的表达，从而延缓IgA肾病的进展。     

IgA肾病患者扁桃体CD4+CD25+T细胞及J链mRNA阳性IgA细胞与临床病理的关系

不少学者认为IgA肾病(IgAN)与扁桃体自身免疫反应有一定联系.IgAN患者扁桃体CD4+CD25+T细胞减少和分泌J链mRNA阳性IgA细胞增多,且CD4+CD25+T细胞数与J链mRNA阳性IgA细胞数呈负相关[1].我们分析其与临床病理的关系.     

Th17细胞在IgA肾病发病机制中的作用

IgA肾病是肾小球系膜区以IgA或IgA沉积为主的原发性肾小球病,是全球范围内最常见的原发性肾小球疾病,约20%~40%的成人患者在20年后会进展为终末期肾病[1].在过去的几十年中,对IgA肾病的研究已经取得了很大的进展,比较明确其临床特点、病理特征、预后等.但对于IgA肾病的发病机制尚未明了.Th17细胞是近来发现的一类新的CD4＋T辅助细胞亚群,是独立于Th1和Th2细胞之外的效应T细胞亚群,其产生的多种相关细胞因子[如IL-17A（IL-17）和IL-17F]在炎症和自身免疫反应起着关键性作用[2].在人类,Th17细胞可以引起多器官炎症反应、风湿性关节炎、炎症性肠病等[3].近年研究发现[4],Th17细胞引起的免疫反应在肾脏炎症性疾病的发病中也起到了重要作用.本文从Th17细胞及其分泌的主要细胞因子IL-17与IgA肾病自身免疫的相关性进行综述.     

补体在IgA肾病发病机制中的研究进展

IgA肾病是一种以肾小球系膜区IgA或IgA为沉积主,常伴补体C3沉积的原发性肾小球疾病.近年来研究表明补体的激活是IgA肾病发生与发展的重要因素,许多临床和实验室资料表明,补体在炎症性疾病发生、发展过程中起着重要的作用.现就IgA肾病与补体之间的关系作一综述.     

肾移植后IgA肾病复发的研究进展

随着免疫抑制治疗的进展,在预防肾移植后急性排斥反应和提高移植物短期及长期生存方面取得了一些进步.但肾移植患者存活时间越长,移植后IgA肾病复发越来越多,并且成为导致移植肾失功的一个重要原因.目前对移植后IgA肾病复发的原因还不明确.在预防及治疗复发性IgA肾病方面,除了ACEI/ARB类药物被认为具有保护肾功能的作用,其他治疗包括免疫治疗仍存在很大的争议.本文就移植后IgA肾病复发的相关原因、预后及治疗进展作一综述.     

Cross-species costimulation: relative contributions of CD80, CD86, and CD40

BACKGROUND: The response of human CD4+ T cells against porcine cells is of comparable magnitude to that induced by human leukocyte antigen-mismatched allogeneic cells. This reflects productive interactions between key costimulatory molecules across the species barrier. Inhibition of these molecular interactions will be crucial in overcoming CD4+ T-cell-mediated rejection of xenografts. We have performed a detailed investigation to determine the expression profiles and relative contributions of the three key costimulatory molecules in the porcine-human xenogeneic response. Whereas only porcine CD86 is constitutively expressed on resting endothelial cells, both CD40 and CD80 are rapidly expressed after activation. All three costimulatory molecules are expressed by professional antigen-presenting cells. METHODS: We have isolated full-length cDNA clones for human and porcine CD80, CD86, and CD40. Human fibroblast cell lines (M1) coexpressing DR1 were transfected with these cDNAs and used in mixed lymphocyte reactions and flow cytometric studies in vitro. RESULTS: These data provide the first characterization of the expression profile and functional role of porcine CD80. Functional assays demonstrate that pCD40, pCD80, and pCD86 are independently capable of costimulating human CD4+ T cells, albeit with differing kinetics. Proliferative responses were of comparable magnitude to those obtained when costimulation was provided by human CD40, CD80, and CD86. CONCLUSIONS: These data have implications for therapy targeting the direct pathway of xenorecognition; costimulatory molecule blockade must be directed against both the B7/CD28 and CD40/CD40L pathways.     

CD52 ligation induces CD4 and CD8 down modulation in vivo and in vitro

To successfully induce donor-specific tolerance after immune depletion, it is essential to understand the residual and recovering immune system in the context of the depleting agent because the properties of such a recovering immune system differ based on the depleting agent used. In this study, we investigate the phenotypic and functional characteristics of T cells exposed to Campath-1H in vivo and in vitro. Recovering T cells demonstrated down modulated surface CD4 and CD8 (by flow cytometry) for up to 45 days after Campath-1H administration. Additionally, these T cells had an activated phenotype. To determine whether this CD4/8 down modulation was due to T-cell activation only or in part due to Campath-1H, whole blood from healthy volunteers was exposed to Campath-1H and the surviving lymphocytes isolated. Flow cytometry revealed a dose-dependent down modulation of CD4/8 without T-cell activation. Additionally, these Campath-1H-treated T cells were immunocompetent as indicated by increased surface CD69 and interleukin-2 (IL-2) production following stimulation by soluble anti-CD3 mAb. In conclusion, Campath-1H by itself down modulates surface CD4 and CD8 without activating T cells.     

CD27/CD70, CD134/CD134 ligand, and CD30/CD153 pathways are independently essential for generation of regulatory cells after intratracheal delivery of alloantigen

BACKGROUND: We investigated whether blockade of tumor necrosis factor receptor-ligand pathways could generate regulatory cells induced by intratracheal delivery of alloantigen. METHODS: CBA (H-2k) mice were pretreated with intratracheal delivery of splenocytes (1x10(7)) from C57BL/10 (H-2b) mice and intraperitoneal administration of monoclonal antibody (mAb) specific for CD70, CD134 ligand (CD134L), CD153, or CD137L. Seven days later, C57BL/10 hearts were transplanted into pretreated CBA mice. Some naive CBA mice underwent adoptive transfer of splenocytes (5x10(7)) from pretreated CBA mice and transplantation of a C57BL/10 heart on the same day. RESULTS: Untreated CBA mice rejected C57BL/10 cardiac grafts acutely (median survival time [MST] 12 days). Pretreatment with intratracheal delivery of C57BL/10 donor splenocytes prolonged graft survival significantly (MST 84 days). Mice given intratracheal delivery of alloantigen plus anti-CD70, anti-CD134L, or anti-CD153 mAb, but not those given intratracheal delivery of alloantigen plus anti-CD137L mAb, rejected their graft acutely (MST 16, 14, 10, and 65 days, respectively). Adoptive transfer of splenocytes from mice pretreated with intratracheal delivery of alloantigen plus anti-CD70, CD134L, or CD153 mAb did not prolong survival of C57BL/10 cardiac grafts in naive secondary CBA recipients (MST 14, 11, and 11 days, respectively), whereas adoptive transfer of splenocytes from mice given intratracheal delivery of alloantigen plus anti-CD137L mAb did (MST 75 days). CONCLUSION: The CD27/CD70, CD134/CD134L, and CD30/CD153 pathways are independently required for generation of regulatory cells in our model.     

Peripheral T-cell lymphomas expressing CD30 and CD15

Coexpression of CD30 and CD15 is typically associated with classic Hodgkin's lymphoma (HL). Peripheral T-cell lymphomas (PTCLs) can often display histologic features that simulate classic HL. However, reports of PTCLs coexpressing both CD30 and CD15 have been infrequently described. We report 11 cases of PTCL in which at least a subset of the neoplastic cells coexpressed CD30 and CD15. The patients included 4 women and 7 men and age ranged from 43 to 83 years (median, 62 years). Nine of 10 patients had advanced stage III or IV disease at presentation. Nodal involvement predominated in 8 of 11 patients, whereas 2 patients presented primarily with skin involvement. Two distinct groups were identified based on morphologic and immunophenotypic features. The first group of 5 cases had histologic features mimicking classic HL with CD30+, CD15+ Reed-Sternberg (RS)-like cells in an inflammatory background of varied extent and composition. The background lymphoid cells showed minimal cytologic atypia. The RS-like cells were negative for CD20 and CD79a in all cases, and CD45 expression was absent in 4 of 5 cases. The RS-like cells expressed CD25 and at least one T-cell-associated marker in all cases. The background T-cell population showed convincing subset predominance in 4 of 5 cases and loss of T-cell-associated antigens in 3 of 5 cases and coexpression of CD30 and CD15 in one case. The second group of 6 cases had morphologic features more in keeping with PTCL than classic HL. The proportion of neoplastic cells coexpressing CD30 and CD15 varied. Loss of T-cell antigens was noted in all cases and CD4 predominated in 4 of 5 cases. Three of the 6 cases expressed CD45. PCR analysis revealed clonal T-cell receptor gamma (TCR-gamma) chain gene rearrangements in 9 of 11 cases, but no immunoglobulin heavy (IgH) chain gene rearrangements. In situ hybridization studies for Epstein-Barr virus were negative in all cases. In some PTCL cases, the overlap with classic HL can be striking, and combined immunophenotypic and molecular studies are often necessary to confirm the diagnosis.     

CD117与CD34在胃肠道间质瘤中的表达

目的探讨胃肠道间质瘤的临床病理和免疫组化特征.方法观察40例间质瘤的病理形态特征,并用免疫组化S-P法检测CD117与CD34的表达情况.结果镜下梭形细胞为主型30例(75%),上皮样细胞为主型8例(20%),混合细胞型2例(5%).免疫组化显示CD117与CD34的阳性率分别为90%和83%,其表达率与肿瘤大小、核分裂数及组织学类型无关.结论联合检测CD117与CD34可以提高间质瘤的诊断准确率,但不能判断良恶性程度.     

系统性红斑狼疮患者外周血单个核细胞CD28及CD80分子表达的研究

目的：探讨ＣＤ２８及ＣＤ８０分子在活跃期ＳＬＥ患者外周血单个核细胞（ＰＢＭＣ）上的表达及在ＳＬＥ发病中的可能作用机制。方法：采用流式细胞仪检测 １３例初发活跃期及 １３例复发活跃期 ＳＬＥ患者ＰＢＭＣ表面 ＣＤ２８及ＣＤ８０分子的表达。结果：初发及复发活跃期ＳＬＥ患者ＰＢＭＣ表达ＣＤ２８分子与正常对照组比较有一定程度的下降，但差异无显著性（Ｐ＞０．０５）。初发活跃期ＳＬＥ患者ＰＢＭＣ表达ＣＤ８０分子较正常对照组明显升高（Ｐ＜０．０５）。初发与复发活跃期ＳＬＥ患者之间比较ＰＢＭＣ表达ＣＤ２８及ＣＤ８０分子无显著性差异（Ｐ＞０．０５）。结论：ＳＬＥ患者外周血Ｔ细胞及ＡＰＣ间存在异常的ＣＤ２８－ＣＤ８０。共刺激分子的信号传导，这种异常的信号传导在ＳＬＥ发病机制中可能起着重要的作用。     

Immunohistochemical analysis of CD83, CD8 and CD4 positive cells in renal cell carcinoma

OBJECTIVES: In order to evaluate the immunological milieu in renal cell carcinoma (RCC), we investigated infiltration by mature dendritic cells (CD83 positive cells), cytotoxic-T cells (CD8 positive cells) and helper-T cells (CD4 positive cells) in RCCs, as well as in surrounding normal tissues and correlations between the cell types. MATERIALS AND METHODS: Specimens from 33 surgically resected RCCs were embedded in paraffin and then stained for CD4, CD8, CD83. Each section contained three areas, tumor tissue, tumor margin and normal renal parenchyma. Cells positive for CD4, CD8 and CD83 were counted each area. RESULT: Cells positive for CD4, CD8 and CD83 were observed predominantly in the tumor margins, rather than tumor tissue and normal renal parenchyma. The differences were significant in the number of immune positive cells between tumor margin and tumor tissue, and between tumor margin and normal renal parenchyma. A significant correlations was found between CD4 and CD83 positive cells (r = 0.805, p < 0.0001), and also between CD8 and CD83 positive cells (r = 0.505, p < 0.0001). CONCLUSION: It has been reported that mature dendritic cells induces cytotoxic-T cell and helper-T cell responses. Infiltrating mature dendritic cells, cytotoxic-T cells and helper-T cells were present only in the tumor margin. This may reflect significant immune reaction around the tumor margin.