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1.
蕈样肉芽肿皮损p55及p75肿瘤坏死因子受体表达   总被引:1,自引:0,他引:1  
p55及p75肿瘤坏死因子受体分布于角朊细胞、淋巴细胞、中性粒细胞及某些肿瘤细胞表面,介导肿瘤坏死因子多种生物学效应[1,2]。为了探讨其在蕈样肉芽肿(MF)皮损中的表达及意义,我们对9例MF皮损进行了免疫组化检测。资料和方法1.病例9例MF中男8例...  相似文献   

2.
为探讨外周血细胞因子的变化与儿童寻常型银屑病发病机理的关系,采用放射免疫分析法检测儿童寻常型银屑病患儿血清中TNFα和IL6水平,采用ELISA法检测IL8的水平,对其相关性进行研究。儿童银屑病组血清中TNFα、IL6、IL8含量均明显高于正常对照组,经t检验分析,两组间具有统计学意义(P<0.01。儿童寻常型银屑病组患儿血清中TNFα与IL6、IL8含量的升高均呈正相关。提示在儿童寻常型银屑病发病中TNFα可能是IL6、IL8升高的重要促进因素,它们有可能互相诱导或存在某种协同作用共同参与了银屑病的炎症性免疫病理过程。  相似文献   

3.
目的 : 探讨肿瘤坏死因子 (TNF)α受体 5 5 0 0 0 (P5 5 )在银屑病皮损和血清中的表达及其意义。方法 : 采用免疫组织化学、RT -PCR和ELISA方法对寻常型银屑病患者皮损表皮P5 5及mRNA表达和血清水平进行了检测。结果 : 正常表皮不表达P5 5及mRNA ;银屑病皮损表皮P5 5及mRNA高表达 ;银屑病患者血清P5 5水平明显高于对照组 (t=3.18,P <0 .0 5 ) ,皮损表皮角质形成细胞P5 5表达强度与其血清P5 5水平呈显著正相关 (r’s=0 .5 82 ,P <0 .0 5 )。结论 : 银屑病患者皮损和血清TNF -α受体P5 5的异常上调 ,可能是银屑病发生和发展的原因之一。  相似文献   

4.
银屑病患者白介素6和肿瘤坏死因子α的测定   总被引:4,自引:1,他引:4  
用生物活性测定法对49例寻常型银屑病患者和20例正常人外周血单一核细胞(PBMC)体外产生白介素6(IL6)和肿瘤坏死因子α(TNFα)的能力及其血清水平进行了测定,并对其相关性进行了分析。结果:患者PBMC产生IL6、TNFα的能力及其血清水平均高于正常人;PBMC产生IL6、TNFα的能力与其血清水平呈正相关;血清IL6与TNFα水平呈正相关。提示:患者的细胞免疫功能存在失调;血清IL6、TNFα水平升高可能与PBMC产生IL6、TNFα能力增强有关;IL6、TNFα在银屑病发病中可能存在协同作用。  相似文献   

5.
目的 研究肿瘤坏死因子α(TNF α)、白介素 6 (IL 6 )和白介素 8(IL 8)在尖锐湿疣发病机理中的作用。方法 采用ELISA双抗体夹心法 ,测定了 2 1例尖锐湿疣患者血浆、内毒素刺激的外周血单一核细胞培养上清液和 1 7例患者疣体组织TNF α、IL 6、IL 8含量。结果 尖锐湿疣患者组的血浆刺激的外周血单一核细胞分泌的TNF α、IL 6、IL 8水平显著低于正常人组 ;疣体组织的IL 6、IL 8水平显著低于正常人组 ;两组组织中TNF α均未能检出。结论 尖锐湿疣患者全身和皮损局部存在着单核 巨噬细胞功能下降 ,而这种功能下降可能是导致尖锐湿疣患者淋巴细胞功能缺陷的重要原因。提高单核 巨噬细胞功能 ,对尖锐湿疣的防治 ,可能具有一定意义  相似文献   

6.
目的研究神经生长因子(nerve growth factor,NGF)受体P75和P140trkA在寻常型银屑病发病机制中的作用.方法应用原位杂交技术检测了33例寻常型银屑病患者(18例为进展期,15例为静止期)和10例正常人皮肤组织中两受体(P75和P140trkA)mRNA的表达情况.结果与正常人皮肤比较,寻常型银屑病皮损及非皮损中P75和P140trkA受体mRNA的表达明显上调,且皮损中的表达明显高于非皮损区(P<0.01);进展期患者皮损与非皮损中P75和P140trkA受体mRNA的表达分别高于静止期患者的皮损与非皮损区(P<0.01).结论神经生长因子及其两受体可能是参与银屑病病理机制的重要因子.  相似文献   

7.
目的探讨肿瘤坏死因子(TNF)α受体75 000(p75)在寻常性银屑病中的作用机制。方法采用免疫组化和ELISA 方法对寻常性银屑病患者皮损、皮损周围“正常”皮肤p75表达及其在血清中的含量进行检测。结果正常人皮肤表皮基底细胞散在表达p75;银屑病患者皮损周围“正常”表皮、皮损表皮、真皮内浸润单一核细胞(MNCs)均表达p75;银屑病皮损表皮角质形成细胞p75表达强度与真皮内MNCs数呈显著正相关(r's = 0.73,P<0.05);银屑病患者血清中p75的含量与对照组比较差异有显著性(t=3.98,P<0.05);银屑病皮损表皮角质形成细胞p75表达强度与其血清中p75含量呈显著正相关(r's = 0.62,P<0.05)。结论银屑病患者皮肤和血清中TNFα受体p75的异常上调可能是造成银屑病发生和发展的原因之一。  相似文献   

8.
9.
目的观察异维A酸对重度痤疮患者肿瘤坏死因子α(TNF-α)和白介素8(IL-8)的影响。方法选择符合条件的重度痤疮患者56例,口服异维A酸胶丸,10mg/次,3次/d,12周为1个疗程,采用ABC-ELISA双抗体夹心法检测服药前后血清中TNF-α和IL-8的水平,另外选择40名非痤疮的健康体检者作为测定指标的正常参考值。结果治疗前重度痤疮患者血清中TNF-α及IL-8的水平均明显高于健康对照组(均P<0.01);治疗后重度痤疮患者血清中TNF-α的水平较治疗前明显降低(P<0.01),但仍明显高于健康对照组(P<0.01);治疗后重度痤疮患者血清中IL-8的水平较治疗前明显降低(P<0.01),但与健康对照组相比,差异无统计学意义(P>0.05)。结论异维A酸能明显降低重度痤疮患者血清中TNF-α及IL-8的水平。  相似文献   

10.
目的:检测白三烯(LTs)、IL-8和TNF-α在银屑病中的表达.方法:采用ELISA方法分别检测32例银屑病患者血清、尿液和皮损中LTB4、LTE4水平及血清、皮损中IL-8和TNF-α水平,并与20例健康志愿者作对照.结果:患者血清、皮损中IL-8、TNF-α和血清、尿液、皮损中LTE4水平均明显高于对照组(均P<0.01),皮损中LTB4水平明显升高(P<0.01),但血清和尿液中LTB4水平与对照组相比差异无显著性(P>0.05).皮损中LTB4、LTE4和IL-8水平与银屑病皮损面积与严重性指数(PASI)评分变化趋势一致,均有显著相关性.结论:白三烯通过参与局部炎症反应在银屑病发病中起重要作用.  相似文献   

11.
目的:探讨肥大细胞和IL-8在寻常型银屑病中的作用。方法:采用免疫组化技术(SABC法)观察寻常型银屑病皮损处MC分布和IL-8在表皮中的表达情况。结果:寻常型银屑病皮损处MC密度明显高于皮肤血管炎组和健康对照组;寻常型银屑病皮损处KC中IL-8的表达明显高于两对照组。结论:结果提示MC和IL-8参与寻常型银屑病的致病过程,并且两者之间存在相关性。  相似文献   

12.
目的:研究在体外商陆皂苷甲(EsA)对银屑病患者外周血单个核细胞(PBMC)分泌肿瘤坏死因子(TNF-α)和可溶性白介素2受体(sIL-2R)水平的影响,探讨其治疗银屑病的可能机制。方法:标本取自30例寻常性银屑病患者和20名健康献血员,利用EsA分别与脂多糖(lipopolysaccharide,LPS)或植物血凝素(phytohemagglutinin,PHA)协同刺激PBMC,用双抗体夹心ABC-ELISA检测PBMC培养上清液中TNF-α和sIL-2R水平。结果:EsA浓度为1.0~10.0μg/mL时,呈剂量依赖性地明显抑制银屑病患者PBMC释放TNF-α(P<0.05)。EsA浓度在0.5~10.0μg/mL时,PBMC分泌sIL-2R呈轻微的下降趋势,但差异无统计学意义(P>0.05),EsA对PHA诱导的sIL-2R释放无显著的抑制作用。结论:抑制TNF-α等炎症递质的释放可能是中国商陆治疗银屑病的机制之一。  相似文献   

13.
目的:探讨甲氨蝶呤(MTX)对银屑病患者血清白介素-8和组胺水平的影响。方法:用酶联免疫吸附实验(ELISA)检测银屑病患者和正常人外周血IL-8水平;用荧光分光光度计测定银屑病患者和正常人外周血组胺水平。结果:(1)治疗前银屑病患者血清IL-8和组胺水平明显高于正常对照组(P<0.01),经MTX治疗后,患者血清IL-8和组胺水平与正常对照组差异无显著性(P>0.05)。结论:抑制组胺的释放和IL-8的分泌,降低中性粒细胞和T淋巴细胞的趋化活性,减轻炎症反应及组织损伤可能是MTX治疗银屑病的作用机制之一。  相似文献   

14.
目的:研究窄谱中波紫外线治疗寻常性银屑病的疗程、近期不良反应及预后;观察照射前后血清细胞因子浓度改变.探讨治疗机制。方法:给予86例寻常性银屑病患者窄谱中波紫外线(NB-UVB)照射,每周3次,共267次,用酶联免疫吸附试验检测32例患者治疗前后血清白介素-8(1L-8)、血管内皮细胞生长因子(VEGF)水平。结果:86例患者治疗后15例痊愈,临床有效率为93.2%,32例患者治疗前血清IL-8水平较健康对照者水平高,照射后显著下降。治疗前仪斑块状银屑病患血清清VEGF水平较正常人为高,照射后显著下降:结论:NB-UVB治疗银屑病疗效高、不良反应少,复发率低、IL-8水平升高可能为寻常性银屑病的发病机制之一。VEGF水平升高可能是斑块状银屑病致病的因素之一。  相似文献   

15.
The distribution of transferrin receptor in normal human skin and its expression in psoriatic skin and various skin tumors have been investigated. Immuno-peroxidase staining was performed on biopsy specimens using monoclonal OKT 9 antibody, which reacts with transferrin receptor. Normal human skin showed positive staining with OKT 9 in eccrine glands and outer root sheaths of the hair. Sebaceous glands were also strongly positive. The basal layer stained very weakly. Psoriatic skin expressed OKT 9 strongly in the epidermis, especially in the area of the rete ridge. In squamous cell carcinoma, Bowen's disease, and malignant melanoma, a widespread and strong labelling reaction was found. Basal cell epithelioma and genital Paget's disease were partially and moderately positive in their staining pattern. No such positive staining pattern could be found in either nevus cell nevi or seborrhoic keratosis. These findings indicate that, in normal skin, transferrin receptor exists in eccrine glands, sebaceous glands, and outer root sheaths of the hair in greater amounts. High amounts of expression of this receptor in psoriatic epidermis and malignant tumors suggests that immunohistochemical demonstration of transferrin receptor parallels the proliferating activity of the tissue or tumor of the skin and may provide an useful aid for detecting such conditions.  相似文献   

16.
Etanercept for the treatment of psoriasis and psoriatic arthritis   总被引:1,自引:0,他引:1  
Etanercept is a fully human soluble recombinant p75 TNF receptor that blocks the binding of TNF to cell surface receptors, thereby neutralizing its biologic activity. Data supporting the FDA's approval of etanercept for controlling signs and symptoms and for inhibiting XRAY progression of psoriatic arthritis will be presented. Data supporting the FDA filing of etanercept for the treatment of moderate to severe psoriasis will also be presented. Long term safety data of etanercept in the over 231,000 adults and children with rheumatoid arthritis who have been treated worldwide will be briefly summarized.  相似文献   

17.
目的:为了探索c-myc及c-jun与银屑病的关系。方法:运用免疫组化SP法对22例寻常型银屑病患者及15例正常人皮肤c-myc及c-jun的表达进行观察。结果:c-myc、c-jun在银屑病皮损中过度表达,而在正常皮肤不表达或弱表达,结论:c-myc、c-jun可能与银屑病的表皮细胞过度增殖、分化异常有关。  相似文献   

18.
The efficacy and safety of infliximab in patients with plaque psoriasis, psoriatic arthritis, pustular psoriasis (excluding localized type) and psoriatic erythroderma were assessed in clinical practice. Without washout of the existing treatment of psoriasis, treatment was switched to infliximab, which was given at a dose of 5 mg/kg at weeks 0, 2 and 6 and then every 8 weeks up to week 46. The primary end-points were 75% improvement in Psoriasis Area and Severity Index score (PASI 75 response rate) for plaque psoriasis, 20% improvement in American College of Rheumatology criteria (ACR 20 response rate) for psoriatic arthritis, and global improvement in pustular psoriasis and psoriatic erythroderma. The PASI 75 response rate in plaque psoriasis was 72.2% at week 10 and 53.6% at week 50. The ACR 20 response rate in psoriatic arthritis was 66.7% at week 14 and 80.0% at week 46. The response defined as global improvement in pustular psoriasis was between 66.7% and 100.0% during the 2–50-week period. The response defined as global improvement in psoriatic erythroderma was between 75.0% and 100.0% during the week-2–50 period. There were 14 discontinued patients. The most frequently reported reason for discontinuation was the development of adverse events. However, there were no serious respiratory diseases, infections or infusion reactions. In patients with plaque psoriasis, psoriatic arthritis, pustular psoriasis and psoriatic erythroderma, infliximab was well tolerated, regardless of prior treatment, and also showed superior efficacy over a period of approximately 1 year.  相似文献   

19.
银屑病测皮损中c-myc和c-jun的检测   总被引:1,自引:0,他引:1  
目的:为了探索c—myc及c—jun与银屑病的关系。方法:运用免疫组化SP法对22例寻常型银屑病患者及15例正常人皮肤c—myc及c—jun的表达进行观察。结果:c—myc、c—jun在银屑病皮损中过度表达,而在正常皮肤不表达或弱表达,结论:c—myc、c—jun可能与银屑病的表皮细胞过度增殖、分化异常有关。  相似文献   

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