系统性红斑狼疮患者血清IL-10的水平及临床意义

目的观察系统性红斑狼疮(systemic lupus erythematosus,SLE)患者血清IL-10的表达与疾病活动的关系。方法选取22例SLE患者及24名健康人作为对照,根据狼疮疾病活动指数(SLE disease activity index,SLEDAI)将SLE患者分为活动期组和非活动期组,检测血清抗dsDNA抗体,血清总补体溶血活性(CH50)及C反应蛋白(C reactive protein,CRP),酶联免疫吸附法(ELISA)检测血清IL-10表达。结果与对照组[(18.11±6.97)ng/L]相比,IL-10在SLE活动期组[(78.54±5.62)ng/L,P<0.01]及非活动期组[(30.36±10.98)ng/L,P<0.05]均有所增高,活动期组增高更为明显(与非活动期组相比,P<0.05)。IL-10水平与SLEDAI呈正相关(SLE活动期,r=0.77,P<0.01;SLE非活动期,r=0.84,P<0.01),IL-10的水平与抗dsDNA抗体(r=0.71,P<0.01)、CRP(r=0.63,P<0.01)和CH50(r=-0.56,P<0.05)均相关。结论IL-10在SLE患者血清中表达升高,在疾病活动时更为明显,IL-10能反应疾病活动的程度,可以做为临床观察SLE疾病活动的指标之一。     

系统性红斑狼疮患者血清IL-18、IL-8水平观察

<正>系统性红斑狼疮(systemic lupus erythematosus,SLE)是一种可累及多种系统、原因不明的自身免疫性疾病。临床表现为血清中出现多种自身抗体,常累及肾脏,引起狼疮性肾炎,最后导致患者死亡[1]。据报道70%的SLE患者有肾脏受损的表现,引发狼疮性肾炎(lupus nephritis,LN),严重者可导致肾功能衰竭[2]。细胞因子异常分泌在SLE发病中发挥着     

系统性红斑狼疮患者血清IL-10和IL-18的检测及意义

目的探讨系统性红斑狼疮（SLE）患者血清IL-10和IL-18的表达及其与疾病活动的关系。方法应用ELISA法检测104例SLE患者和100例健康体检者血清IL-10和IL-18的水平,其中SLE患者根据疾病活动性指数（SLEDAI）评分标准分为活动组（56例）和缓解组（48例）,比较各组结果的差异,并分析SLEDAI与IL-10和IL-18的相关性。结果 SLE组IL-10和IL-18水平分别为（18.25±3.66）、（582.61±65.28）pg/ml,明显高于对照组的（7.12±2.36）、（186.24±60.39）pg/ml,差异有统计学意义（P〈0.01）;SLE活动组IL-10和IL-18水平分别为（25.98±4.75）、（683.72±62.48）pg/ml,高于缓解组的（14.67±3.21）、（493.51±69.17）pg/ml,差异亦有统计学意义（P〈0.01）;SLE患者血清IL-10和IL-18水平与SLEDAI呈正相关（P〈0.05）。结论 IL-10和IL-18在SLE发病机制中发挥重要作用,而且与疾病活动性相关。     

IL-10RA基因多态性及其与系统性红斑狼疮关系的研究

目的:确定SLE模型小鼠IL-10RA基因变异及其与SLE表现型是否存在关联。方法:用微卫星遗传标记及数量性状位点(QTL)分析方法确定SLE模型小鼠B/W F1的SLE易感基因精确染色体定位并选取候选易感基因,对候选易感基因进行测序分析,选取有基因序列异常的候选易感基因进行PCR-SSCP分析,确定候选易感基因碱基序列变异位点与抗染色质抗体、抗DNA抗体,抗组蛋白抗体及蛋白尿等SLE表现型的相关关系。结果:QTL分析结果表明B/W F1×NZB小鼠抗染色质抗体易感基因与NZW型IL-10RA基因紧密连锁;测序分析发现IL-10RA基因编码区有18处碱基变异,其中7处碱基变异将导致编码氨基酸的变异;抗染色质抗体、抗DNA抗体,抗组蛋白抗体及蛋白尿等SLE表现型与NZW型IL-10RA基因密切相关。另一种SLE模型小鼠MRL的IL-10RA基因存在相同变异。结论:NZW小鼠IL-10RA基因编码区碱基序列存在变异,B/W F1×NZB小鼠SLE表现型与NZW小鼠第9染色体IL-10RA编码区碱基变异相关,提示IL-10RA可能是SLE模型小鼠的一个SLE易感基因。     

系统性红斑狼疮患者血清白细胞介素-18水平变化的意义

目的探讨系统性红斑狼疮（SLE）中白细胞介素-18（IL-18）的表达及其临床意义。方法应用双抗体夹心酶联免疫吸附实验（ELISA）方法分别测定50例SLE患者血浆的IL-18水平。结果SLE患者血清IL-18水平增高,活动期组较稳定期组增高明显（P〈0．05）,与正常对照组比较差异具有显著性（P〈0．05）。SLE患者治疗后IL-18水平低于治疗前水平（P〈0．05）。结论SLE患者血清IL-18水平显著增高,与SLE的病情活动密切相关,检测IL-18对SLE病情的判断有一定的价值。     

IL—10在系统性红斑狼疮发病机制中的角色

系统性红斑狼疮的B细胞过度活化,细胞介导的免疫应答受损。而IL－10既是有效的B细胞刺激因子,又能抑制T细胞和抗原递呈细胞的功能,在SLE发病机制的免疫调节紊乱中扮演重要角色：IL－10的基因与SLE易感性有关,在SLE病人的健康亲属体内IL－10也呈高表达,该因子还参与疾病状态下的细胞因子谱偏移及细胞凋亡异常。IL－10分泌增加与狼疮环境的形成密切相关。     

系统性红斑狼疮患者治疗前后血清TNF-α、IL-6和sIL-2R水平变化及临床意义

目的:探讨系统性红斑狼疮( SLE)患者治疗前后肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和可溶性白细胞介素-2受体(sIL-2R)的水平变化及对免疫功能的影响。方法:采用固相酶标记化学发光免疫分析技术检测40例SLE患者激素治疗前后血清TNF-α、IL-6和sIL-2R水平,应用免疫速率散射比浊法测定免疫球蛋白G(IgG)和补体3(C3)水平。以30例体检正常者作对照。结果:40例SLE患者治疗前活动期血清IgG、TNF-α、IL-6和sIL-2R水平明显高于正常对照组,而C3水平明显低于正常对照组,均P0.01。经激素治疗后(稳定期),SLE患者血清IgG、TNF-α、IL-6和sIL-2R水平显著下降,C3显著升高,均P0.01,但IgG、C3、TNF-α和IL-6水平仍与正常对照组有显著统计学差异(P0.01)。结论:SLE患者TNF-α、IL-6和sIL-2R表达增加,提示SLE的发病过程涉及免疫紊乱和细胞因子失平衡。     

系统性红斑狼疮患者血清IL-18、sVCAM-1和VEGF水平及其意义

目的探讨白细胞介素18（IL-18）、可溶性血管黏附分子-1（sVCAM-1）和血管内皮生长因子（VEGF）水平变化与系统性红斑狼疮（SLE）发病机制的关系。方法采用酶联免疫ELISA法检测SLE患者35例,正常对照组25例血清IL-18、sVCAM-1和VEGF的水平。结果SLE组IL-18（521．23±134．29）pg／mL、sVCAM-1（1179．25±225．57）ng／mL、VEGF（198．85±41．96）pg／mL,较正常对照组IL-18（256．39±59．52）pg／mL、sVCAM．1（538．16±91．21）ng／mL、VEGF（125．62±32．15）pg／mL明显升高,差异有统计学意义（P均〈0．01）。活动期SLE患者IL-18（687．44±158．60）pg／mL、sVCAM．1（1478．14±322．72）ng／mL、VEGF（236．25±48．62）pg／mL与非活动期组sLEIL—18（355．02±109．98）pg／mL、sVCAM-1（881．37±128．30）ng／mL、VEGF（160．47±35．79）pg／ml之间比较,差异有统计学意义（P均〈0．01）。结论SLE患者IL-18、sVCAM-1和VEGF水平增高,且与疾病的活动性相关。     

系统性红斑狼疮患者血清泌乳素水平的检测及其临床意义

目的：探讨系统性红斑狼疮(SLE)患者血清泌乳素(PRL)水平检测的临床意义。方法：应用免疫放射量度分析法测定了75例SEE患者与25例健康人血清PRL水平。结果：SLE患者血清PRL水平明显高于正常对照组，且活动期升高更明显；高泌乳素血症(HPRL)发生率为40％，伴HPRL的患者肾损害发生率明显高于血清PRL正常者；血清PRL水平与SLEDM评分、抗ds-DNA抗体滴度倒数呈正相关，与C3呈负相关。结论：SLE患者血清PRL水平升高与病情活动相关，其检测可作为监测狼疮病情活动性的指标之一；血清PRL水平升高与肾脏损害相关，提示PRL可能在SLE肾损害中起作用。     

血清泌乳素与系统性红斑狼疮患者肾损害的相关性

目的: 探讨系统性红斑狼疮（SLE）患者血清PRL水平与肾损害的相关性。方法： 应用免疫放射量度分析法检测80例SLE患者血清PRL水平并分析其与肾受累的关系。 结果： 高泌乳素血症者肾受累发生率明显高于PRL水平正常者，血清PRL水平与SLEDAI评分、抗ds-DNA抗体滴度、24 h尿蛋白定量、尿微量白蛋白定量（MA）、尿转铁蛋白定量（MTF）、尿免疫球蛋白定量（Ig）及肾脏病理活动指数呈正相关，与血清白蛋白(ALB)水平呈负相关。Logistic 回归分析显示肾受累与血清PRL水平增高及C3水平降低有关。结论： 血清PRL水平升高与SLE肾脏受累有关，其检测可作为肾脏受累的监测指标之一。     

The expression of PD-1 and level of CXCL10 in patients with systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is known tobe a chronic and complicated rheumatic diseasewith an autoimmune etiology.SLEis also a proto-type of autoimmune disease due to a substantialoverlapinits clinical symptoms withother autoim-mune diseases . The immune systemof SLElosesbalance of auto-tolerance ,in which lymphocytesare activated excessively,contributingto SLE de-velopment .It has been well established that effi-cient T cell-mediated immune responses requirenot only the TCR-mediat…     

Association between polymorphisms at the human IL-10 locus and systemic lupus erythematosus

Recent studies have shown elevated IL-10 levels in several rheumatic autoimmune diseases, and particularly in systemic lupus erythematosus (SLE). Such changes may have a genetic basis. We studied two novel polymorphic dinucleotide repeats in the IL-10 promoter region (IL 10.G and IL 10.R) in order to investigate their possible significance in association with this condition in a group of 56 Caucasian SLE patients compared with 102 ethnically matched controls. The results show that there is an allelic imbalance between SLE patients and controls at the IL 10.G microsatellite; this observation is supported by a significant difference in genotype distribution. The nature of autoantibody production and the presence or absence of renal involvement also appeared to be associated with certain IL 10.G microsatellite alleles, although the small size of individual clinical sub-groupings may have influenced this result. No association with the IL 10.R microsatellite was observed. Overall, the differences observed at the IL 10.G microsatellite between SLE patients and controls suggest that the IL-10 locus contributes to the genetic background important for the development of this disease. Although the moderate sample size described in this study requires that the results be interpreted carefully, they provide an interesting and useful framework for future study.     

Serum IL-10 from systemic lupus erythematosus patients suppresses the differentiation and function of monocyte-derived dendritic cells

The role played by cytokines,other than interferon(IFN)-α,in the differentiation and function of dendritic cells(DCs) in systemic lupus erythematosus(SLE),remains unclear.Serum interleukin-10(IL-10) levels are generally elevated in SLE patients,which might modulate the differentiation of DCs.In this study,DCs were induced from monocytes either by transendothelial trafficking or by culture with granulocyte-macrophage colony-stimulating factor(GM-CSF) + IL-4 + tumor necrosis factor(TNF)-α.Both systems were used to investigate the effects of elevated serum IL-10 level on DC differentiation in SLE patients.The results showed that monocyte-derived DCs induced by either SLE serum or exogenous IL-10 reduced the expression of human leukocyte antigen(HLA)-DR and CD80,decreased IL-12p40 level,and increased IL-10 level,and exhibited an impaired capacity to stimulate allogenic T-cell proliferation.These results indicate that serum IL-10 may be involved in the pathogenesis of SLE by modulating the differentiation and function of DCs.     

重建系统性红斑狼疮治疗与创面修复的平衡

复习目前国内外关于系统性红斑狼疮合并皮肤溃疡的病例报道及基础研究,探讨系统性红斑狼疮合并皮肤溃疡的临床特点及治疗方法.皮肤溃疡的严重程度不仅与局部创面相关,同时也与全身病情严重程度密不可分,对于此类皮肤溃疡需要多学科协作,定期评估创面局部情况与全身病情进展程度,及时调整治疗方案,寻找控制病情与创面修复的平衡点.     

IL-10 production in B cells is confined to CD154+ cells in patients with systemic lupus erythematosus

The immunological hallmark of SLE is B cell hyperactivity. CD154 (CD40-L) is normally expressed in activated T cells, and plays an important role in T-B interactions. Its expression is increased in SLE T cells. Additionally, its expression on B cells leads to the development of SLE-like disease in a transgenic model. IL-10 is a key cytokine in the disturbed SLE immune system. The aim of this work was to explore the relation between IL-10 and CD154 expression in SLE B cells. We studied 11 SLE patients and 10 healthy volunteers. Mononuclear cells were isolated from peripheral blood and cultured in the presence or absence of Cowan I Strain Staphylococcus (CSS). Surface CD154 and intracytoplasmic IL-10 expression were quantified with flow cytometry. In basal conditions, CD154 expression was not different in patients and controls. B cell stimulation did not cause a significant increase in CD154 expression in control B cells. However, its expression increased 2 times in B cells obtained from SLE patients. IL-10 expression was confined to CD154(+) cells. Our results show that IL-10 production is intimately linked to CD154 expression in B cells, and that the IL-10(+)CD154(+) B cell subset increases abnormally when SLE-derived cells are stimulated with CSS.     

系统性红斑狼疮患者外周血单个核细胞中IL—4和IL—13 mRNA的表达

目的探讨Th2型细胞因子在系统性红斑狼疮(SLE)发病机制中的作用及其意义.方法应用逆转录-聚合酶链反应(RT-PCR)检测了34例活动期SLE患者和30例正常人外周血单个核细胞(PBMC)中IL-4和IL-13mRNA的表达水平.结果活动期SLE患者IL-4和IL-13的阳性表达率与正常人对照组相比均无明显差异(P>0.05);活动期SLE患者PBMC中IL-4和IL-13mRNA的平均表达水平(0.938 6±0.168 9,0.898 3±0.115 3)均明显高于正常人对照组(0.5494±0.151 0,0.608 5±0.090 3),差异非常显著(P<0.001).结论Th2型细胞因子IL-4和IL-13在SLE患者中呈高水平表达,这可能与SLE患者外周血T细胞高度活化、功能异常有关.     

系统性红斑狼疮患者骨髓间充质干细胞细胞因子分泌及其与病情活动的相关性研究

目的 探讨系统性红斑狼疮（SLE）患者骨髓间充质干细胞（MSCs）细胞因子分泌及其与疾病活动的相关性.方法 采用密度梯度离心和贴壁分离法对11例SLE患者和6例正常人骨髓MSCs进行分离培养,流式细胞术鉴定MSCs.取P2代细胞,半定量RT-PCR检测SLE患者骨髓MSCs白细胞介素-6（IL-6）,IL-7,IL-11,巨噬细胞集落刺激因子（M-CSF）和干细胞因子（SCF）的表达.结果 SLE患者MSCs均表达CD29、CD44和CD105,不表达CD14、CD34、CD45和HLA-DR.两组P2代MSCs均表达IL-6、IL-7、IL-11、M-CSF和SCF.SLE患者组MSCs IL-6、IL-7表达降低（P＜0.01）,IL-7的表达和SLE的活动评分（SLEDAI）呈负相关（r=-0.891,P＜0.05）.结论 SLE患者MSCs细胞因子分泌异常,可能与SLE血液系统损害及病情活动相关.