寻常性银屑病患者血清中MIF和VEGF的表达

目的探讨巨噬细胞移动抑制因子(MIF)和血管内皮生长因子(VEGF)与寻常性银屑病的关系。方法用人MIF,VEGF的ELISA试剂盒分别测定40例银屑病患者和17例正常人血清中MIF和VEGF值。结果寻常性银屑病患者MIF水平明显高于正常对照组(P<0.01),进行期患者高于静止期(P<0.01);进行期寻常性银屑病患者VEGF水平高于静止期(P<0.01)及正常对照组;寻常性银屑病患者血清中MIF水平与PASI评分成正相关,而VEGF水平与PASI评分无相关性(P>0.05);寻常性银屑病患者血清中MIF与VEGF水平呈正相关性(P<0.05)。结论寻常性银屑病患者血清MIF和VEGF水平明显改变,二者可能在寻常性银屑病发病机制中起重要作用。     

寻常性银屑病患者血清巨噬细胞移动抑制因子和血小板源生长因子的表达

目的:探讨巨噬细胞移动抑制因子(MIF)和血小板源生长因子(PDGF)与寻常性银屑病的关系.方法:用人MIF和PDGF的ELASA试剂盒分别测定40例银屑病患者和17名正常人血清中MIF和PDGF值.结果:寻常性银屑病患者MIF水平明显高于正常对照组(P<0.01),进展期患者水平高于静止期(P<0.01);进展期寻常性银屑病患者PDGF水平高于静止期(P<0.01)及正常对照组;寻常性银屑病患者血清中MIF和PDGF水平与银屑病皮损面积和严重度指数(PASI)评分成正相关;寻常性银屑病患者血清中MIF与PDGF水平呈正相关(P<0.05).结论:寻常性银屑病患者血清MIF和PDGF水平明显改变,二者可能在该病发病机制中起重要作用.     

0.1％他克莫司软膏对斑块状银屑病皮损MIF表达的影响

目的 探讨银屑病皮损中巨噬细胞移动抑制因子（Macrophage migration inhibition factor,MIF）的表达水平及其相关性,并比较他克莫司对银屑病皮损中MIF的影响,讨论其临床意义.方法 采用免疫组化法和染色评分半定量法对50例进行期斑块状银屑病皮损标本和42例正常皮肤组织标本（对照组）中的MIF的表达量进行检测,比较结果.同时,选取30例对他克莫司治疗有效的银屑病消退期皮损中MIF的表达量与曲安奈德治疗组、安慰剂治疗组各30例及未用药组50例进行比较.结果 斑块状银屑病皮损中MIF的表达量明显高于对照组,2组间差异有统计学意义（P＜0.05）.他克莫司和曲安奈德药物治疗组MIF的表达阳性率明显减低（P＜0.05）,安慰剂组与未用药组的MIF表达阳性率无统计学意义（P＞0.05）.结论 斑块状银屑病皮损中MIF的表达与疾病的严重程度相关,他克莫司可以明显抑制MIF在银屑病皮损中的表达,达到与糖皮质激素相当的治疗效果,他克莫司对银屑病的治疗作用可能与其抑制MIF的表达有关。     

吡硫翁锌气雾剂对寻常型银屑病患者血清MIF和VEGF的影响

吡硫翁锌能有效抑制表皮角质形成细胞的过度增殖,并能抑制皮脂过度分泌,有抑菌作用,可减轻皮损处的炎性反应,缓解皮损处的瘙痒及疼痛.我们应用吡硫翁锌治疗银屑病,并检测患者血清巨噬细胞移动抑制因子(MIF)和血管内皮生长因子(FEGF)的变化,报道如下.     

麻风的淋巴细胞和巨噬细胞在巨噬细胞移动抑制试验中的表现

作者对氨苯砜或氯苯吩嗪(B_(663))治疗的16名结核样型病人、22名瘤型病人以及18名健康人,进行了巨噬细胞移动抑制试验,观察在有特异性抗原——麻风菌苗(Leprolin)时麻风的淋巴细胞和巨噬细胞(麻风病人的血中单核细胞)的表现,即在麻风菌苗的刺激下,麻风病人的淋巴细胞产生巨噬细胞移动抑制因子(MIF)的能力和麻风病人的巨噬细胞对MIF反应的能力。巨噬细胞移动抑制的程度用移动指数表示。     

Expression of MIF, COX-2 and VEGF in psoriatic lesions and its significance

目的:探讨巨噬细胞移动抑制因子(macrophage migration inhibitory factor,MIF)、环氧化酶-2 (cycloxygenase-2,COX-2)及血管内皮生长因子(vascular endothelial growth factor,VEGF)与进行期寻常性银屑病的关系.方法:采用免疫组化SP方法,分别检测30例进行期寻常性银屑病患者皮损组织及10例正常皮肤组织中MIF、COX-2及VEGF的表达,并进行相关分析.结果:30例进行期寻常性银屑病患者皮损中MIF的平均吸光度(MA)值为0.32±0.03,COX-2的平均A 值为0.31±0.02,VEGF的平均A 值为0.30±0.05,以上3个因子在进行期寻常性银屑病患者皮损组织中的表达水平均显著上调,与对照组相比差异均有系统学意义(P < 0.05).以上3种因子之间存在正相关关系,相关系数r 值分别为0.82、0.81、0.78(P < 0.05).结论:进行期寻常性银屑病患者皮损中MIF、COX-2及VEGF表达水平明显改变,该3种因子可能在银屑病发病机制中起作用.     

药疹时的巨噬细胞移动抑制因子

巨噬细胞移动抑制因子(MIF)是在相应的抗原刺激后出致敏的T淋巴细胞释放的一种淋巴因子,与细胞免疫有关.已报道MIF试验对一些不同类型不良药物反应的病例、以及对数例由不同种     

大疱性类天疱疮患者血清与疱液中巨噬细胞游走抑制因子的检测

目前认为大疱性类天疱疮(BP)的发病不仅与自身抗体的产生有关,而且与细胞因子网络的紊乱密切相关.巨噬细胞游走抑制因子(macrophage migration inhibitory factor,MIF)作为一种前炎症因子,在细胞因子网络平衡中发挥一定作用.本研究采用ELISA方法检测BP患者活动期血清、疱液中MIF的含量和缓解期血清中MIF的含量,以探讨MIF在BP发病机制中的作用及其临床意义.     

大疱性类天疱疮患者血清与疱液中巨噬细胞游走抑制因子的检测

目前认为大疱性类天疱疮(BP)的发病不仅与自身抗体的产生有关,而且与细胞因子网络的紊乱密切相关.巨噬细胞游走抑制因子(macrophage migration inhibitory factor,MIF)作为一种前炎症因子,在细胞因子网络平衡中发挥一定作用.本研究采用ELISA方法检测BP患者活动期血清、疱液中MIF的含量和缓解期血清中MIF的含量,以探讨MIF在BP发病机制中的作用及其临床意义.     

大疱性类天疱疮患者血清与疱液中巨噬细胞游走抑制因子的检测

目前认为大疱性类天疱疮(BP)的发病不仅与自身抗体的产生有关,而且与细胞因子网络的紊乱密切相关.巨噬细胞游走抑制因子(macrophage migration inhibitory factor,MIF)作为一种前炎症因子,在细胞因子网络平衡中发挥一定作用.本研究采用ELISA方法检测BP患者活动期血清、疱液中MIF的含量和缓解期血清中MIF的含量,以探讨MIF在BP发病机制中的作用及其临床意义.     

Local Cytokine Expression in Steroid-Modified Tinea Faciei

In tinea faciei, a dermatophyte infection of the face, early stage lesions show erythema with crust and/or vesicles, a condition often misdiagnosed as dermatitis. Steroid application retards the healing in some cases and may induce penetration of the dermatophyte hyphae into hair and hair follicles. In the present study, we examined local immunity mediated by cytokines derived from lesional T lymphocytes in late stage of this disease. Interferon-gamma (IFN-γ) and macrophage migration inhibitory factor (MIF) were highly expressed, but neither interleukin-4 (IL-4) nor interleukin-5 (IL-5) could be detected by RT-PCR using cryosections. These data suggested that IFN-γ and MIF may be important in the delayed-type hypersensitivity (DTH) response against the fungus in the hair follicle in late stages.     

巨噬细胞移动抑制因子与皮肤病相关性的研究进展

巨噬细胞移动抑制因子是一种前炎症因子,可由多种细胞产生,它既是一种细胞因子,又是一种源于垂体的激素,还可以作为糖皮质激素生理活动的负反馈调节剂。随着巨噬细胞移动抑制因子cDNA的成功克隆及其结构的阐明,巨噬细胞移动抑制因子的特殊生物学活性及其在多种疾病中的重要作用已日益为人们所重视。巨噬细胞移动抑制因子的功能是抑制巨噬细胞游走,在多种皮肤疾病的发生发展中,巨噬细胞移动抑制因子起到了重要的始动及促进作用。     

Detection of migration inhibitory factor (MIF) by a monoclonal antibody in the microvasculature of inflamed skin

Summary Macrophage migration inhibitory factor (MIF) is known as a mediator of cellular immunity with specific effects on the differentiation of mononuclear phagocytes. There is little information on the production of MIF in vivo and its role in the pathophysiology of inflammation. We studied the distribution of MIF in various tissues with a monoclonal antibody against human MIF (1C5/B) using the indirect immunoperoxidase method. Here, we investigate the expression of MIF on endothelial cells of dermal vessels. Our results show that dermal vessels may constitutively express MIF and can be strongly activated to express MIF in acute inflammations such as eczema and psoriasis in contrast to the chronically infiltrated skin from patients with pseudolymphomas and sarcoidosis. In these cases a possibly MIF defective state of vessels and a restriction of positive vessels to distinct anatomical sites of the inflamed skin was detected. The significance of the described association of MIF with vascular endothelium is still a matter of speculation. MIF expression on endothelium may provide an important differentiogenic signal for mononculear phagocytes on their way to the tissue site.     

MACROPHAGE MIGRATION INHIBITORY FACTOR (MIF) IN GUINEA PIGS AND HUMANS WITH DELAYED HYPERSENSITIVITY

When lymph node cells from PPD-sensitive guinea pigs were incubated with PPD for 20–24 hours, they produced a soluble mediator which inhibited the migration of normal guinea pig peritoneal exudate cells (GP-PEC) out of capillary tubes. Also, human lymphocytes stimulated by antigen produced a soluble mediator which inhibited migration of normal GP-PEC and peripheral leukocytes. Guinea pig migration inhibitory factor (MIF) was eluted in the 34,000–67,000 molecular weight (MW) region of cultured supernatants. Human MIF was harvested from the 25,000 MW region of cultured supernatants from human lymphocytes fractionated on Sephadex G-100. Intradermal injection of the MIF into normal guinea pigs provoked reactions characterized by erythema and induration. The histologic response was found to be similar to that induced by antigen injection into sensitized animals. MIF from antigen stimulated lymphocytes may not have species specificity between guinea pig and human, although their molecular weights are different. No correlation was found between delayed skin reactivity induced by antigen in vivo and MIF production in vitro, and it is suggested that a substance inhibitory to MIF activity may be released in the lymphocyte culture.     

Macrophage migration inhibitory factor gene polymorphism is associated with psoriasis

Macrophage migration inhibitory factor (MIF), an important pro-inflammatory cytokine, is over-expressed in plaques of psoriasis and increased levels are found in the sera of patients with psoriasis. Promoter polymorphisms of the MIF gene are associated with increased production of MIF and have been found to confer increased risk of susceptibility to chronic inflammatory diseases. We investigated whether there is an association between promoter polymorphisms of the MIF gene and chronic plaque psoriasis. Two hundred and twenty-eight UK caucasian patients with chronic plaque psoriasis, and a control panel of 401 UK caucasian normal volunteers were studied. MIF promoter polymorphisms were genotyped by allelic discrimination, or by a fluorescently labeled primer method, and capillary gel electrophoresis. Carriage of either the MIF-173*C polymorphism or the MIF CATT(7) polymorphism was positively correlated with psoriasis (odds ratios (OR) 1.52 95% confidence intervals (CI) 1.05-2.19 (p=0.024) and OR 1.67 95% CI 1.1-2.5 (p=0.013), respectively. The OR for presence of the CATT(7)-MIF-173(*)C haplotype versus all other haplotypes combined was 1.69 95% CI 1.2-2.5 (p=0.008). The results provide evidence for polymorphisms in the MIF gene, and in particular the CATT(7)-MIF-173(*)C haplotype, being of importance in susceptibility to psoriasis.     

斑秃患者外周血单一核细胞中Th1/Th2型细胞因子的表达

【摘　要】:目的:探讨斑秃患者外周血单一核细胞(PBMC)中Th1/Th2型细胞因子的表达状况与斑秃发病的关系。方法:用逆转录—聚合酶链反应(RT-PCR)分别检测18例轻型斑秃、24例重型斑秃患者及20例正常人外周血单一核细胞(PBMC)经PHA刺激后具有代表性的Th1型细胞因子：γ干扰素（IFN-γ）和肿瘤坏死因子β（TNF-β）和具有代表性的Th2细胞因子白介素4（ IL-4）、白介素10（IL-10）的表达水平。结果:经PHA刺激后轻型斑秃患者PBMC中Th1型细胞因子(IFN-γ、TNF-β)基因表达水平明显升高,与正常对照组比较有显著性差异(P<0. 05);Th2型细胞因子(IL-4、 IL-10)基因表达水平下降,显著低于正常对照组(P<0. 05);重型斑秃患者PBMC中Th1型细胞因子(IFN-γ、IL-12)基因表达不仅显著高于正常对照组(P<0. 05),而且还高于轻型斑秃病人(P<0. 05);Th2型细胞因子(IL-4、IL-10)基因表达显著低于正常对照组(P<0. 05),与轻型斑秃病人比较有显著性差异。结论:斑秃患者PBMC中Th1/Th2型细胞因子基因表达失衡,表现以Th1型细胞因子基因过度表达为特征的Th1型反应,可能参与了斑秃的发病机制。 关键词:斑秃;细胞因子;基因表达; γ-干扰素; 肿瘤坏死因子-β; 白介素-4 ; 白介素-10 ;外周血单个核细胞;     

硬皮病皮损中巨噬细胞游走抑制因子的表达

目的:检测巨噬细胞游走抑制因子在硬皮病中的表达.方法:免疫组化方法检测巨噬细胞游走抑制因子在20例硬皮病患者皮损中的表达,以10名正常人皮肤组织为对照.结果:硬皮病皮损中巨噬细胞游走抑制因子表达明显高于正常对照组.结论:巨噬细胞游走抑制因子表达增强可能与硬皮病的发病有关.     

Role of macrophage migration inhibitory factor (MIF) in the skin

Macrophage migration inhibitory factor (MIF) functions as a pleiotropic protein, participating in both inflammation and immune responses. MIF was originally discovered as a lymphokine involved in delayed type hypersensitivity and various macrophage functions, including phagocytosis, and tumor surveillance. Recently, MIF has been re-evaluated as a pro-inflammatory cytokine and identified as a pituitary-derived hormone, potentiating endotoxemia. MIF is ubiquitously expressed in various tissues, including the skin. Clinical evidence of increased MIF expression in inflammatory diseases supports this potential role of MIF in inflammation. In addition to its role in inflammation, MIF has been shown to exhibit growth-promoting activity, with anti-MIF antibodies effectively suppressing tumor growth and tumor-associated angiogenesis. This review presents the latest findings on the roles of MIF in the skin with regard to inflammation, the immune response, skin disease, tumorigenesis and cutaneous wound healing, and discusses its potential functions in various pathophysiological states.