尿毒症病人循环单核细胞Fas的表达及血浆FasL水平

目的：慢性肾功能衰竭（肾衰）病人单核细胞功能低下与其凋亡加速有关,兹拟进一步探讨尿毒症病人单核细胞凋亡加速的机制。方法：对7例尿毒症未透析病人和18例液透析（血透）病人进行观察,以15例正常人为对照。采用流式细胞仪检测单核细胞Fas和Fas配基（Fas ligand,FasL）的表达;以ELISA法测定血浆中可溶性FasL（sFasL)的水平。在体外将单核细胞与重组人FasL共同孵育,抽提DNA后用碘化丙啶染色、流式细胞仪检测单核细胞凋亡率,四甲基偶氮唑蓝（MTT）法观察单核细胞存活率。结果：尿毒症未透析病人和血透病人单核细胞Fas的表达较正常人明显上调（P＜0.05）;血透病人的Fas表达水平高于非透析病人（P＜0.05）。正常人和尿毒症病人的单核细胞表面均未检测出FasL表达。正常人血浆中未能检测出sFasL,但尿毒症病人血浆中存在有sFasL;sFasL的水平在尿毒症未透析病人和血透病人之间、血透病人透前与透后之间、以及采用聚砜膜和纤维素膜透析器进行透析的两者之间差异均无显著性（P＞0.05）。单核细胞与重组人FasL在体外共同培养2h后,血透病人单核细胞的凋亡率较正常人明显增高,而其存活率则较正常人明显低下。结论：尿毒症病人单核细胞表面功能Fas表达上调,血浆中存在sFasL,这可能是慢性肾衰病人单核细胞凋亡的原因之一。     

胃癌及癌旁组织Fas、Fas L的表达

目的：探讨细胞凋亡相关蛋白的Fas、FasL在胃癌发生、发展中的作用。方法：对74例手术切除胃癌标本，应用免疫组化S－P法检测Fas、FasL蛋白在癌组织和相应癌旁组织中的表达。结果：在高中分化型胃癌Fas和FasL的阳性表达率一致性显著高于低分化型胃癌（P＜0．05）。而在早期和进展期胃癌间，有淋巴结转移和无淋巴结转移胃癌间Fas和FasL的阳性表达率无显著性差异（P＞0．05）。胃癌组织Fas 阳性表达率显著低于癌旁组织（P＜0．05）。FasL在两者间无显著性差异（P＞0．05）。结论：Fas和FasL的异常表达可能是胃粘膜癌变过程中细胞凋亡抑制的重要机制之一，并与胃癌的分化和免疫逃逸有关。     

Fas/FasL途径在柔红霉素诱导HL-60及U937细胞凋亡中作用的研究

目的；研究柔红霉素（DNR）诱导白血病细胞凋亡的机制，进一步探讨Fas/FasL 途径在DNR诱导白血病细胞凋亡中的作用。并评价sFAsL与DNR联用的致凋亡效应。方法：将DNR作用于白血病细胞系HL－60，K562，U937细胞，并用流式细胞术（FCM）检测其Fas抗原表达的改变。sFasL,DNR诱导白血病细胞凋亡，以抗Fas单抗（IgG1)阻断Fas/FasL 途径，借助原位末端标记法（TUNEL）和FCM检测白血病细胞凋亡率。结果：DNR处理HL－60，K562，U937细胞18h后，Fas表达阳性率无明显变化（P＞0．05），与sFasL联合作用后显示出协同效应，。IgG1不能阻断DNA致白血病细胞凋亡的作用，但可阻断sFasL致白血病细胞凋亡的作用。结果：DNR致白血病细胞株U937，HL－60凋亡的作用不依赖于Fas/FasL 途径，但sFasL与DNR联合应用可协同增强抗肿瘤效应。     

肝癌组织中凋亡调控因子Fas、FasL及caspase-3的表达及意义

目的：探讨凋亡调控因子Fas、FasL及caspase-3在肝细胞癌（HCC）组织中的表达及其临床意义。方法应用免疫组织化学SP法检测80例HCC患者肝癌组织及其相应癌旁正常肝组织中Fas、FasL及caspase-3的表达,并分析其表达与 HCC临床病理因素的相关性。结果 Fas、FasL及caspase-3在 HCC、癌旁组织中的表达比较,均差异有统计学意义（P＜0．05）。在TNM 分期（Ⅲ～Ⅳ期）、有门静脉癌栓、有淋巴结转移的肝癌组织中Fas 的阳性表达率明显降低（P＜0．05）;在病理分级（Ⅲ～Ⅳ级）、TNM分期（Ⅲ～Ⅳ期）、有门静脉癌栓、有淋巴结转移的肝癌组织中FasL的阳性表达率明显增高（P＜0．05）;在病理分级（Ⅲ～Ⅳ级）、TNM分期（Ⅲ～Ⅳ期）、有淋巴结转移的肝癌组织中 caspase-3的阳性表达率明显降低（P＜0．05）。80例 HCC患者肝癌组织中Fas、FasL与caspase-3的表达,两两之间并无明显关联性（狉＝0．057,P＞0．05）。结论 Fas/FasL系统的失衡及caspase-3低表达导致肝癌细胞凋亡障碍,在 HCC发生、发展及转移中起着重要作用。     

Fas、FasL在慢性乙型肝炎患者肝细胞和外周血淋巴细胞上的表达

探讨慢性乙型肝炎患者肝细胞及外周血淋巴细胞上Fas、FasL的表达与乙型肝炎病毒（HBV）复制水平及肝组织炎症程度的关系。对30例慢性乙型肝炎患者进行肝穿刺肝组织病理检查及免疫组化SP法检测肝细胞中Fas、FasL表达强度。并采用单克隆抗体经流式细胞仪检测外周血淋巴细胞上Fas、FasL表达阳性百分率；同时，采用荧光实时标记法测定血清中病毒复制指标HBV DNA水平；采用Beckman全自动生化分析仪检测肝功能并研究其相关性。慢性乙型肝炎患者肝细胞中Fas、FasL表达强度随肝组织炎症活动度加重而增强（P均〈0．001），与白蛋白及丙氨酸转移酶（ALT）呈负相关（P〈0．005，P〈0．001），与球蛋白、总胆红质无明显相关性（P均〉0．05）。外周血淋巴细胞上Fas、FasL的表达阳性率与血清中肝炎病毒复制指标HBV DNA水平呈正相关；与慢性肝炎分度无明显的相关性。乙型肝炎病毒感染可诱导肝细胞及外周血淋巴细胞上Fas、FasL的表达。肝细胞Fas、FasL的表达随炎症活动度加重而表达增强，但其介导的凋亡并不引起肝细胞炎症损伤即ALT活性并不升高，相反减少；同时在某种程度上影响白蛋白的合成。提示Fas—FasL介导的肝细胞凋亡是以非细胞损伤方式参与慢性乙型肝炎的发病过程。同时，随血清HBV DNA水平增高，外周血淋巴细胞上Fas、FasL的表达亦增强，淋巴细胞的凋亡因而增多，是导致乙型肝炎慢性化的原因之一。由此可见，Fas、FasL介导的凋亡参与了慢性乙型肝炎的发病机制，且在慢性乙型肝炎的发生发展中起重要作用。     

幽门螺杆菌感染对Fas/FasL表达的影响在胃癌发生中的作用

目的：观察幽门螺杆菌（Hp）及其不同毒力株（cagA阳性与cagA阴性株）感染对胃黏膜上皮细胞Fas/FasL表达的影响，进而探讨胃癌的发生机制。方法：胃镜下取胃窦黏膜标本，将研究对象按病理结果分为黏膜萎缩组，黏膜萎缩伴轻度不典型增生组，黏膜萎缩伴中度不典型增生组，胃腺癌组，黏膜大致正常组为对照组，再根据Hp感染情况为分Hp阳性组与阴性组，并将Hp阳性组进一步成cagA阳性组及阴性组，共9组80例。以快速尿素酶试验，PCR及组织学第三种方法检测Hp，用PCR方法对Hp进行分型。用免疫组化法检测Fas、FasL等表达情况。结果Hp感染率为60．0％，cagA阳性率为90．47％，非腺癌病人Hp阳性组Fas/FasL表达明显高于Hp阴性组（P＜0．05），腺癌组Fas/FasL表达明显高于大致正常组及黏膜萎缩，黏膜萎缩伴轻度不典型增生，黏萎缩伴中度不典型增生组（P＜0．01）。cagA阳性组Fas/FasL表达与cagA阴性组差异无显著性（P＞0．05）。结论：幽门螺杆菌感染后早期即黏 萎缩阶段已出现Fas、FasL等的表达增加，随细胞凋亡的增加，黏膜上皮细胞萎缩加重，细胞DNA不稳定性增加，并出现不典型增生加重， Fas、FasL的表达随之增强，一旦肿瘤细胞形成，Fas/FasL表达进一步增加，形成局部免疫豁免区，导致肿瘤的浸润生长。cagA阳性的菌株在促成肿瘤的发生过程中无明显作用。     

系统性红斑狼疮患者外周血TB淋巴细胞Fas FasL表达及与凋亡的关系研究

目的探讨系统性红斑狼疮(SLE)患者外周血T、B淋巴细胞Fas、FasL表达及与凋亡的关系.方法采用流式细胞术(FCM)检测了30例SLE活动期患者、30例SLE非活动期患者和30名正常人外周血T、B淋巴细胞的凋亡率及Fas、FasL表达率.结果T、B淋巴细胞的Fas表达率依次为:活动期组＞非活动期组＞正常对照组(P＜0.01);FasL的表达率除B淋巴细胞在SLE活动期显著高于正常对照组外(P＜0.01),其余各组间差异无统计学意义;细胞的凋亡率在活动期显著高于非活动期(P＜0.01),而非活动期与正常对照组差异无统计学意义(P＞0.05):SLE的活动性与T或B细胞的Fas、FasL表达率间无相关关系,而与T或B细胞的凋亡率呈正相关(P＜0.01);无论是T或B细胞,Fas、FasL的表达率与凋亡率间无相关性.结论SLE患者体内外周血淋巴细胞的凋亡受到多种因素影响,但最终仍表现为凋亡率的异常增高,特别是活动期SLE,推测外周血淋巴细胞凋亡率的增高在SLE发病机制中起着重要作用.     

Fas、FasL蛋白在非小细胞肺癌组织的表达及其生物学意义

目的探讨Fas和FasL蛋白在非小细胞肺癌（NSCLC）的表达及其生物学意义。方法应用免疫组化法对45例NSCLC和25例癌旁正常肺组织中Fas和FasL蛋白表达进行检测。结果①与受检正常肺组织Fas表达相比，NSCLC Fas表达明显下调（P〈0．05）；Fas表达与NSCLC组织类型及分化程度有关（P〈0．05，P〈0．01）。②FasL表达与NSCLC组织类型、分化程度、临床分期及淋巴结转移有关（P〈0．01，P〈0．05）。NSCLC Fas与FasL表达无相关关系，NSCLC瘤团或癌巢周边区与中央区FasL表达差异显著。结论Fas和FasL异常表达在NSCLC发生、发展及转移过程中起重要作用。     

急性冠脉综合征患者血浆可溶性Fas配体水平变化及其意义

目的：探讨急性冠脉综合征患者血浆可溶性Fas配体（sFasL）水平的变化及其意义。方法：入选急性冠脉综合征患者50例,其中急性心肌梗塞（AMI）30例（AMI组）、不稳定型心绞痛（UAP）20例（UAP组）,另有稳定型心绞痛（SAP）患者20例为SAP组,30例健康对照者为健康对照组。采用酶联免疫吸附试验检测各组sFasL水平,并比较其结果。结果：（1）血浆sFasL水平在AMI组[（100.56±30.61）pg/ml]和UAP组[（51.13±23.46）pg/ml]显著高于SAP组[（7.08±1.20）pg/ml]和健康对照组[（6.19±1.11）pg/ml],P均〈0.01;（2）病程观察显示AMI患者经皮冠状动脉成形术后3h内血浆sFasL水平迅速下降,此后再次上升,而SAP患者则否;（3）冠状窦内sFasL水平明显高于外周血[（210±40）pg/ml∶（78±21）pg/ml,P〈0.05];（4）体外研究表明FasL信使核糖核酸表达在AMI患者离体单核细胞上调,低氧可刺激离体单核细胞sFasL释放。结论：急性冠脉综合征患者sFasL水平显著升高提示Fas/FasL系统活化,可能参与急性冠脉综合征的发病过程。     

系统性红斑狼疮患者T细胞上Fas受体分子数与治疗效果的相关性

目的 通过定量流式细胞术检测系统性红斑狼疮（SLE）患者T淋巴细胞表面Fas受体的分子数（Fas/T），探讨其对疾病治疗效果的指导作用。方法 36例活动期SLE患者，分别给予泼尼松、甲泼尼龙、环磷酰胺冲击治疗，在入院3d内、出院时（平均住院天数为22．6d）和出院后4周复诊时，采集患者外周血，采用Fas定量流式细胞试剂盒荧光染色，通过流式细胞仪对T淋巴细胞上表达Fas受体分子数（Fas/T）进行检测。结果 活动期SLE患者随着皮质类固醇或免疫抑制剂治疗，到出院时T细胞表面Fas/T呈明显升高；出院后4剧复诊时T细胞表面Fas/T呈下降趋势；各组间差异均有统计学意义（P〈0．05）。SLE患者治疗前后T细胞表面Fas/T与SLE疾病活动指数（SLEDAl）之间，具有明显的相关性（P〈0．05），治疗前后T细胞表面Fas/T与抗dsDNA抗体、C3和C4之间无明显的相关性（P〉0．05）。结论 SLE患者T淋巴细胞表面Fas／T与SLE的活动性呈正相关，可作为一种评价SLE疾病活动性的指标，对临床治疗效果具有一定指导作用。由Fas介导的淋巴细胞凋亡是引起SLE免疫功能紊乱的主要原因，也是判断狼疮活动的重要指标。     

Increased circulating levels of soluble Fas ligand are correlated with disease activity in patients with fibrosing lung diseases

OBJECTIVE: The Fas-Fas ligand (FasL) pathway is one of the important apoptosis-signalling molecule systems. We previously determined that this pathway may be involved in the pathogenesis of fibrosing lung diseases. In the present study, we evaluated the clinical significance of the levels of soluble forms of Fas (sFas) and FasL (sFasL) in serum from patients with fibrosing lung diseases. METHODOLOGY: We measured sFas, sFasL, KL-6 (a measure of alveolar type II cell damage), surfactant protein D (SP-D), and surfactant protein A (SP-A) levels in serum from 35 patients with idiopathic pulmonary fibrosis (IPF), 17 patients with interstitial pneumonia associated with collagen vascular diseases (CVD-IP), and 13 normal healthy controls using enzyme-linked immunosorbent assays (ELISA). RESULTS: The serum levels of sFasL were significantly increased in patients with active IPF and CVD-IP, compared with those with inactive disease and controls. There was no significant difference in sFasL levels between patients with inactive disease and controls. Serum sFasL levels were significantly correlated with lactate dehydrogenase and KL-6 levels in IPF. The decrease in sFasL levels following corticosteroid therapy was not correlated with the clinical course of IPF. There was no significant difference in serum sFas levels between IPF or CVD-IP patients and controls. CONCLUSIONS: Although further studies need to be performed on a large number of patients with histologically proven IPF or CVD-IP, it would seem that serum sFasL levels may reflect the activity of IPF and CVD-IP.     

Overexpression of HBxAg in hepatocellular carcinoma and its relationship with Fas／FasL system

AIM: To study the expression and serum level of HBxAg,Fas and FasL in tissues of HCC patients, and to assess the relationship between HBxAg and Fas/FasL system.METHODS: Tissues from 50 patients with HCC were tested for the expression of HBxAg, Fas and FasL by S-P immunohistochemistry. Serum levels of sFas/sFasL and HBsAg/HBeAg were measured by ELISA assay. HBV X gene was detected by PCR in serum and confirmed by automatic sequencing. Fifty cases of liver cirrhosis and 30 normal controls were involved in serum analysis.RESULTS: The expression of HBxAg, Fas and FasL in carcinoma tissues was 96 %, 84 % and 98 %, respectively.Staining of HBxAg, Fas and FasL was observed predominately in cytoplasms, no significant difference was found in intensity between HBxAg, Fas and FasL (P＞0.05). HBxAg, Fas and FasL might express in the same area of carcinoma tissues and this co-expression could be found in most patients with HCC. The mean levels of sFas in serum from HCC, cirrhosis and normal controls were 762.29±391.56 μg@ L-1 835.36±407.33 μg@L-1 and 238.27±135.29 μg@L-1. The mean levels of sFasL in serum from HCC, cirrhosis and normal controls were 156.36±9.61iμg@ L-1, 173.63±18.74 μg@L-1 and 121.96±7.83 μg@ L-1.Statistical analysis showed that both sFas and sFasL in HCC and cirrhosis patients were significantly higher than those in normal controls (P＜0.01). Serum HBV X gene was found in 32 % of HCC patients and ,46 % of cirrhotic patients.There was no significant relationship between serum level of sFas/sFasL and serum X gene detection (P＞0.05). Eight percent of HCC patients with negative HBsAg and HBeAg in serum might have X gene in serum and HBxAg expression in carcinoma tissues.CONCLUSION: Our data suggest that HBxAg and Fas/FasL system plays an important role in the development of human HCC. Expression of HBxAg can leads to expression of Fas/FasL system which and reverse apoptosis of hepatocellular carcinoma induced by FasL.     

Relationship between HBxAg and Fas/FasL in patients with hepatocellularcarcinoma

AIM To assess the relationship between HBV X-gene, X-gene product and Fas/ FasL which mediatehepatocellular apoptosis in patients with hepatocellular carcinoma.METHODS Tissue from 34 patients with hepatocellular carcinoma was tested for the expression of HBxAg.Quantitative ELISA assay was used to detect sFas; and sFasL and PCR were used to detect the HBV X-genein sera from 30 patients with hepatocellular carcinoma, 32 patients with liver cirrhosis and 20 normalcontrols.RESULTS The positive expression of HBxAg, Fas and FasL in carcinoma tissue was 97.06%, 85.29% and100%, respectively. The positive signal was mainly presented in the plasma, and all of these three positivestaining may appear in the same area. Redit analysis showed that there was no significant difference amongthese three positive staining (P >0.05). The mean levels of sFas in sera from hepatocellular carcinoma, livercirrhosis and normal controls were 722.97±321.12, 801.90±419.94 and 224.07±148.23, respectively,showing that sFas levels in patients with hepatocellular carcinoma and liver cirrhosis were significantlyelevated than that in normal controls (P < 0.0l). The mean levels of sFasL in sera from hepatocellularcarcinoma, liver cirrhosis and normal controls were 152.27±7.99, 162.97±12.40 and 154.99 ± 6.96,showing that sFasL level in patients with liver cirrhosis was significantly higher than that in patients withhepatocellular carcinoma and normal controls (P< 0.01). HBV X-gene was found to be positive in sera of30% patients with hepatocellular carcinoma; HBV X-gene was found to be positive in sera of 43.75% ofpatients with liver cirrhosis. There was no significant difference in sFas/sFasL level between HBV X-genepositive patients and HBV X-gene negative patients (P >0.05).CONCLUSION The expression of HBxAg and Fas/FasL in the tissue of hepatocellular carcinoma seemed tobe almost the same, but relation between cause and effect is unclear. The detection of sFas and sFasL inpatient sera may reflect the state of apoptosis mediated by Fas/FasL system. Our data showed that HBV X-gene expression in sera seemed to have no relation to sFas/sFasL level; however, these data also suggestedthat some patients with negative HBsAg in sera might have integrated HBV X-gene in liver tissues, andtherefore X-gene is detectable in those patient sera.     

Transfection of apoptosis related gene Fas ligand in human hepatocellular carcinoma cells and its significance in apoptosis

AIM: To evaluate the expression of apoptosis related gene Fas ligand (FasL) in human hepatocellular carcinoma (HCC) cells HepG2 and its significance in apoptosis. METHODS: Levels of soluble Fas ligand (sFasL) in a group of patients with hepatitis B virus (HBV)-induced chronic hepatitis, HBV-positive liver cirrhosis and HCC were evaluated. In a further study, the recombinant eukaryotic expression plasmid pcDNA3.1hisB-FasL was transfected into HCC cells HepG2 by lipofection, and then soluble FasL was examined in the supernatant of culture cells by EIA, FasL expression in HepG2 cells was detected by immuohistochemistry. After being stained by annexin V and propidium iodine, cells were passed through a flow cytometer and examined by a fluorescence microscope and a laser scanning microscope. RESULTS: The sFasL levels were significantly lower in patients with HCC when compared to the patients with hepatitis or liver cirrhosis. In comparison with untransfected cells, the soluble FasL could be detected in the supernatant of transfected cells. FasL was expressed on the membranes and cytoplasm of transfected cells. The apoptotic cell rate was 36.30% in transfected cells, and was 11.53% in untransfected cells. Moreover, the different stage of apoptotic cells could be distinguished by annexin V and propidium iodine staining. CONCLUSION: Fas ligand is an apoptotic pathway of HCC cells.     

Expression of Fas receptor and soluble Fas ligand (sFasL) concentration in acute leukemia

Apoptosis mediated by the interaction of cytotoxic T lymphocyte with blast cell via Fas receptor/Fas ligand (FasL) pathway is a one of the mechanisms of immunological leukemia surveillance. There is few data on possible blocking of Fas receptor by soluble form of Fas (sFasL) present in serum and the role of blast cells as the source of this ligand. Forty-eight patients with de novo diagnosis of acute leukemia, 32 with myeloblastic (AML) and 16 with acute lymphoblastic leukemia (ALL) were studied. Fas expression on bone marrow leukemic blasts was determined by flow cytomertic immunofluorescent analysis and serum concentration of sFasL assessed at presentation, in remission and in relapse. Blasts of all patients expressed Fas at variable degree (0.8 to 100%). Fas expression was significantly higher on myelo--than on lymphoblasts. There was no relation between degree of Fas expression at diagnosis and remission rate. Concentration of sFasL in acute leukemia patients at diagnosis was significantly higher than in healthy control group, decreased to normal values in remission and rose again in relapse. There was a negative correlation between Fas expression on blasts and sFasL concentration at the time of diagnosis. Results obtained suggest that blast cells could be the source of soluble FasL in acute leukemia patients and that sFasL serum concentration could be used for monitoring of disease activity.     

Cord blood soluble Fas ligand and pediatric atopic dermatitis

Keratinocyte apoptosis is a key pathogenetic mechanism in atopic dermatitis (AD). Fas and Fas ligand (FasL) interaction is an important pathway to induce apoptosis. However, the relationship between early life soluble FasL (sFasL) and AD still is not clear. This study was designed to evaluate if sFasL is associated with the development of AD in children. We performed a nested case-control study within a prospective Taiwan birth-panel cohort study. Umbilical cord blood and maternal plasma samples were gathered at birth. During follow-up, using the International Study of Asthma and Allergies in Childhood questionnaires, we identified 40 AD cases, which we matched to 80 unaffected controls chosen from this cohort. The concentrations of sFasL and immunoglobulin E in plasma were determined by enzyme-linked immunosorbent assay. The relationship of sFasL levels and AD was estimated by mix model. Receiver operating characteristic (ROC) curves were generated to see how well sFasL could predict AD. Cord blood sFasL levels were significantly higher in the AD patients than in the controls (p = 0.003). The concentration of sFasL in the cord blood was higher than in the maternal blood (p < 0.001). There also existed a correlation between the concentration of sFasL in the maternal blood and the cord blood (r = 0.23; p = 0.01). The subjective severity of AD was positively correlated with sFasL levels (r = 0.34; p = 0.02). Cold blood sFasL may be a biomarker in detecting pediatric AD (area under the ROC curve = 0.64). Our results showed a relation between cord blood sFasL and the development of AD in children.     

狼疮肾炎患者外周血淋巴细胞凋亡调控因子和血清尿白细胞介素-8的变化

目的探讨外周血淋巴细胞(PBL)凋亡调控因子和白细胞介素-8(IL-8)在活动性狼疮肾炎(LN)患者中的作用及其临床意义。方法对36例活动性LN患者PBL细胞凋亡调控因子Fas抗原、Fas配体、bcl-2和IL-8进行检测分析,并以15名正常自愿者为对照。Fas、FasL、bcl-2的表达水平运用免疫组织化学法测定。血清、尿IL-8用放射免疫法检测。结果活动性LN患者Fas、FasL、bcl-2表达均显著高于正常人(P<0.001),Fas、FasL表达与临床活动指数呈正相关(r=0.473、P<0.005;r=0.493,P<0.05),bcl-2表达与临床活动指数无显著相关性(r=0.063,P>0.05);血清、尿IL-8水平明显低于正常组(P<0.01),但与临床活动指数无关(r=0.038,P>0.05;(r=0.272,P>0.05),与Fas、FasL、bcl-2无明显相关关系。结论Fas、FasL、bcl-2的表达升高导致外周血淋巴细胞凋亡异常,可能为系统性红斑狼疮(SLE)、LN发病机制之一,PBL中Fas、FasL表达水平可作为病情活动的指标;血、尿IL-8水平低下,可能与免疫功能紊乱有关,有待进一步研究。