Serum Levels of IL-4, IL-10, IL-12, IL-13 and IFN-gamma in Behçet's disease

Behçet's disease (BD) is an inflammatory disease of unknown etiology. Although its pathogenesis is not fully understood, recent studies have suggested that immunological abnormalities and neutrophil hyperfunction may be involved in its etiology and pathophysiology. The immune system in BD can be characterized as a divergent cytokine production profile of the mixed Th1/Th2 cell type. In this study, we investigated the levels of interleukin (IL)‐4, IL‐10, IL‐12, IL‐13 and interferon‐γ in the sera of patients with BD, in comparison with recurrent aphthous stomatitis and healthy controls, to determine the Th1/Th2 profile of the disease. The levels of IL‐4, IL‐10 and IL‐13 were found to be high in active BD patients, and IL‐12 and interferon‐γ levels were lower in active BD patients than in inactive BD, recurrent aphthous stomatitis, and control patients.     

湿疹患者血中IL-2,IL-5,IL-10和EOS的检测及意义

目的探讨湿疹与IL-2,IL-5,IL-10和EOS(嗜酸性粒细胞)的关系。方法采用双抗夹心法(ABC-ELISA法)和直接计数法分别检测湿疹患者60例和正常健康体检者40例的血清IL-2,IL-5,IL-10和血液中EOS的水平,应用SPSS11.5统计软件包对结果作统计学分析。结果湿疹患者IL-2的值低于正常人,而IL-5,IL-10的值和EOS的值高于正常人,P均<0.05,有统计学意义。结论IL-2,IL-5,IL-10和EOS可能参与了湿疹的发病。     

荨麻疹患者外周血淋巴细胞亚群和IL-15,IL-21,IgE检测

目的探讨外周血T,B,NK淋巴细胞亚型及血清白细胞介素(IL)-15,IL-21,IgE变化与荨麻疹发病机制的关系。方法用流式细胞仪检测急性荨麻疹(AU)、慢性荨麻疹(CU)患者和健康献血者外周血CD3+,CD4+,CD8+T细胞、B细胞、NK细胞的构成比,并用ELISA法检测血清IL-15,IL-21,IgE水平,分析其与病情、病程的关系。结果 AU患者的外周血T,B,NK淋巴细胞亚型与正常对照组间差异无显著性(P0.05);CU患者CD4+/CD8+比值、NK细胞高于对照组,而CD8+低于对照组(P0.05),AU和CU组血清IL-15,IL-21水平均低于对照组(P0.01),血清IgE相反(P0.05);AU患者的CD8+T细胞高于CU患者,CD4+/CD8+比值低于CU患者(P0.01),余未见明显区别。CU患者的CD3+,CD8+T细胞与症状评分呈负相关,B细胞与症状评分、病程呈正相关,IgE与IL-21均呈负相关;而AU患者未见明显相关。结论 AU,CU患者存在血清IL-15,IL-21和IgE水平的异常,CU患者还存在外周血T,B,NK淋巴细胞亚型的异常。这些异常可能是荨麻疹发病因素之一,其相互作用还可能引起CU反复发作。     

湿疹患者血清中IL-10,IL-12p40及IL-18水平检测

目的观察湿疹患者血清IL-10,IL-12p40及IL-18的水平,探讨其在湿疹发病机制中的作用和临床意义。方法应用酶联免疫吸附试验(ELISA)法分别检测14例急性期湿疹患者、19例非急性期湿疹患者和15例正常对照者血清中IL-10,IL-12p40及IL-18的水平。结果①血清IL-10水平急性湿疹组低于对照组,非急性湿疹患者组高于对照组(P<0.05)。②血清IL-12p40水平急性湿疹组与非急性湿疹组均高于对照组,且非急性湿疹组高于急性湿疹组(P<0.05)。③血清IL-18水平急性湿疹组与非急性湿疹组均高于对照组(P<0.05),急性湿疹组与非急性湿疹组差异无显著性意义(P>0.05)。结论湿疹患者体内可能存在Th1/Th2型细胞因子分泌紊乱。     

尖锐湿疣患者血清IL-18,干扰素γ和IL-10水平检测

目的探讨尖锐湿疣(CA)患者治疗前、后血清白细胞介素18(IL-18)、干扰素γ(IFN-γ)和白细胞介素10(IL-10)的水平变化在CA免疫发病机制中的作用。方法采用酶联免疫吸附法(ELISA)分别检测42例CA患者在治疗前和治疗后3个月未复发时血清IL-18,IFN-γ和IL-10的水平,并与35例正常人作比较。结果 CA患者治疗前血清IFN-γ明显低于正常对照组(P<0.01),IL-10和IL-18水平明显高于正常对照组(P均<0.01);治疗后3个月末血清IL-18,IFN-γ和IL-10的水平同正常对照组相比,差异无统计学意义(P均>0.05),IL-18和IL-10水平明显低于治疗前(P均<0.01),IFN-γ的水平明显高于治疗前水平(P<0.01)。结论人乳头瘤病毒感染可造成患者细胞免疫功能异常,IL-18,IFN-γ和IL-10在CA免疫发病机制中可能起重要作用。     

IL-10,IL-6及IL-6受体基因多态性与皮肤黑素瘤易感性的关系

目的 探讨白介素10(IL-10)、白介素6(IL-6)及其受体(IL-6R)基因多态性与黑素瘤易感性的关系.方法 收集30例黑素瘤患者和30例健康时照者的外周血样本进行基因型分析.对于IL-6及IL-6R,选择11种单核苷酸多态性(SNPs),并且每种SNPs分为杂合子组、纯合子变异体组和野生型组进行分析.对于IL-...     

银屑病皮损组织中HSP60,HSP90与IL-2,IL-6的检测分析

目的探索银屑病皮损组织中热休克蛋白60(HSP60)、热休克蛋白90(HSP90)与IL-2和IL-6的相关性。方法采用免疫组化法检测银屑病患者皮损组织中HSP60,HSP90,IL-2和IL-6的表达,并进行相关性分析。结果银屑病皮损组织中HSP60,HSP90,IL-2和IL-6均有明显表达;HSP60与IL-2相关系数r=0.44715,P=0.1951,HSP60与IL-6相关系数r=0.70999,P=0.0214,HSP90与IL-2相关系数r=0.52172,P=0.1219,HSP90与IL-6相关系数r=0.72386,P=0.0175。结论银屑病皮损组织中HSP60,HSP90与IL-6的表达有明显的正相关性,与IL-2的表达无相关性,HSP60和HSP90可能在银屑病发病和病程演变中起一定作用。     

慢性自发性荨麻疹血清脱氢表雄酮硫酸酯与总IgE,IL-2,IL-4,IFN-γ的相关性

目的通过研究慢性自发性荨麻疹(CSU)患者与健康对照组血清脱氢表雄酮硫酸酯(DHEA-S)及总IgE,IL-2,IL-4,IFN-γ水平的差异,探讨CSU患者外周血DHEA-S是否与总IgE、Th1/Th2细胞失衡相关。方法 162例CSU患者为实验组,68例健康人为对照组。应用放射免疫分析法测定血清中DHEA-S水平;采用ELISA法检测外周血总IgE,IL-2,IL-4,IFN-γ水平。采用t检验和直线相关性分析分析各组检测值。结果 CSU组外周血DHEA-S,IL-2,IFN-γ水平明显低于健康对照组,血清总IgE,IL-4水平明显高于健康对照组,差异有统计学意义(P0.05)。CSU病情分级与DHEA-S水平呈负相关,与总IgE水平呈正相关(r=-0.664,-0.419,P均0.01),与IL-2,IL-4,IFN-γ水平无明显相关性。CSU组DHEA-S与IL-2,IFN-γ呈显著正相关,与IgE,IL-4呈显著负相关(r=0.409,0.397,-0.319,-0.367,P均0.001)。结论 CSU患者体内可能存在内分泌免疫系统失衡,外周血DHEA-S水平下降可能与总IgE水平升高及Th1/Th2细胞失衡相关。     

梅毒血清固定患者外周血中IL-17,IL-10表达及意义

目的检测梅毒血清固定患者外周血中白细胞介素-17(IL-17)和白细胞介素-10(IL-10)的表达,并探讨其意义。方法分别选取梅毒血清固定患者、初诊梅毒患者、梅毒治疗后非梅毒螺旋体抗原转阴者和健康人各30例,分别记为A组、B组、C组和D组,分别采用酶联免疫吸附试验对各组血清IL-17和IL-10进行检测,对比组间差异。结果四组血清IL-17水平对比差异均无统计学意义(P0.05),且每两组间血清IL-17水平对比差异也均无统计学意义(P0.05);四组血清IL-10水平对比差异有统计学意义(P0.05),且D组血清IL-10水平最高,B组其次,C组稍低,A组最低。结论在梅毒血清固定患者中外周血IL-17水平无明显变化,IL-10水平异常降低,可将其作为梅毒感染及临床疗效的辅助判断指标。     

甲氨蝶呤对寻常性银屑病患者血清IL-23,IL-17水平影响

目的探讨甲氨蝶呤(MTX)治疗寻常性银屑病(PV)的疗效及对患者血清IL-23,IL-17的影响,进一步阐明MTX治疗PV的作用机制。方法应用ELISA方法检测42例寻常性银屑病患者经MXT治疗前后血清IL-23,IL-17水平变化,并与41例正常对照组比较。结果 MTX治疗寻常性银屑病疗效显著,治疗后PASI评分显著下降(P0.01)。患者血清IL-23,IL-17水平分别为(1581.16±463.31)ng/L和(7.44±2.36)ng/L,显著高于正常对照组的(832.41±309.16)ng/L和(2.93±0.85)ng/L,差异有统计学意义(P0.01)。MTX治疗后患者血清IL-23,IL-17水平分别为(845.68±385.95)ng/L和(3.04±0.79)ng/L,与治疗前相比显著下降,差异有统计学意义(P0.01),且患者血清IL-23,IL-17水平与银屑病PASI评分均呈显著正相关(P0.01)。结论 MTX治疗寻常性银屑病疗效显著,可能通过调节Th17细胞降低血清IL-23,IL-17水平发挥治疗作用。     

BALB/c小鼠系统感染白念珠菌血清IL-18,IL-4,IFN-γ的动态变化

目的探讨BALB/c小鼠系统感染白念珠菌后IL-18,IL-4,IFN-γ的动态变化。方法BALB/c小鼠随机分成4组:高菌量感染组,低菌量感染组,免疫功能低下组,正常对照组。分别于系统感染白念珠菌1,4,7天后应用ABC-ELISA检测各组小鼠的IL-18,IL-4,IFN-γ的水平。结果IL-18水平从感染第1天骤降后(但仍高于免疫功能低下组,P<0.05~0.001),至感染后第7天达正常水平;而IFN-γ始终高于正常对照组及免疫功能低下组(P<0.05);IL-4于感染1天后低于正常对照组(但仍高于免疫功能低下组,P<0.05~0.001),感染4天后则与正常对照组差异无显著性,7天后高于正常对照组(P<0.05)。结论高低菌量白念珠菌感染的BLAB/c小鼠,免疫系统早期多以Th1型细胞应答为主;后期Th1/Th2型细胞因子均升高,表明细胞免疫和体液免疫均参与了抗白念珠菌感染。     

小鼠念珠菌性阴道炎模型中TSLP表达及其与IL-2,IL-10关系

目的探讨胸腺间质淋巴细胞生成素(thymic stromal lymphopoietin,TSLP)在小鼠念珠菌性阴道炎发病机制中的作用。方法采用皮下注射雌二醇和阴道内接种白念珠菌悬液建立Balb/c小鼠念珠菌性阴道炎模型,用激光扫描共聚焦显微镜和ELISA检测实验组和对照组小鼠阴道组织中TSLP,IL-2,IL-10表达。结果实验组小鼠阴道组织中TSLP表达明显高于对照组(P0.01);IL-2水平在接种后7d明显增加(P0.01),14d时出现明显下降(P0.01);IL-10含量在接种后7d、14d均明显高于对照组(P0.01)。TSLP仅与IL-10表达呈显著正相关(P0.01)。结论 TSLP表达上调可能在念珠菌致病中起重要的免疫调节作用。     

二期梅毒患者血清IL-17,IL-23和ROR-γt的检测

目的检测二期梅毒患者血清IL-17,IL-23和维甲酸受体相关孤儿受体γt(ROR-γt)的水平,探讨Th17细胞在梅毒免疫致病机制中的可能作用。方法采用酶联免疫吸附法检测30例二期梅毒患者和20例正常人血清IL-17,IL-23和ROR-γt水平。结果 30例二期梅毒患者血清IL-17,IL-23和ROR-γt水平分别为(24.8±20.9)pg/mL,(32.1±8.3)pg/mL和(120.2±40.6)pg/mL,均较健康对照[(12.7±14.2)pg/mL,(21.0±8.7)pg/mL,(72.0±41.8)pg/mL]明显升高(P<0.05)。梅毒患者血清IL-17,IL-23和ROR-γt水平与RPR滴度间无线性相关(P>0.05)。结论梅毒患者血清IL-17,IL-23和ROR-γt水平的升高可能与梅毒的免疫致病机制有关。     

IL-17: Important for Host Defense,Autoimmunity, and Allergy?

In this issue, Milovanovic and colleagues present evidence that IL-17a enhances IgE production, although the precise mechanism remains unclear. Their initial finding was that higher numbers of IL-17a-producing CD4(+) T cells were observed after polyclonal stimulation in a largely airway allergic population. These data add to the evidence that atopic disorders such as asthma and, possibly, atopic dermatitis (AD) may have distinct immunologic phenotypes. The hope is that by characterizing the immunologic basis of these common diseases we will be able to understand the heterogeneity observed in natural history, response to treatments, susceptibility to infections, genetic risk factors, and associations with other atopic disorders.     

Podoplanin expression in wound and hyperproliferative psoriatic epidermis: regulation by TGF-β and STAT-3 activating cytokines, IFN-γ, IL-6, and IL-22

Background

Podoplanin (PDPN)/T1α/aggrus/PA2.26 antigen, a transmembranous glycoprotein, is a well-known lymphatic endothelial marker. Recent evidence indicates that PDPN is also expressed in keratinocytes especially of sebaceous glands.

Objective

To verify expression-pattern and the regulatory mechanism of PDPN in human epidermal keratinocytes.

Methods

PDPN-expression pattern was analyzed in normal and psoriatic epidermis by immunostaining. The regulatory mechanism of PDPN-expression of keratinocytes by cytokines was analyzed using specific inhibitors, siRNA, and adenoviral shRNA of signaling pathways.

Results

In normal skin, PDPN was expressed on the basal cell layer of sebaceous glands and on the outer root sheath of hair follicles. While no expression was detected in the normal interfollicular epidermis, PDPN was detected in the basal cell layer of wound and hyperproliferative psoriatic epidermis, where the granular layer is lacking. TGF-β1 and IFN-γ independently upregulated PDPN-expression of keratinocytes via TGF-β receptor-Smad pathway and JAK-STAT pathway, respectively. IL-6 and IL-22 also stimulated PDPN-expression of keratinocytes accompanied by STAT-3 phosphorylation. siRNA of STAT-1, inhibitors of STAT-3 signaling, AG490, STAT-3 inhibitor VI, and si/shRNA of STAT-3 inhibited the PDPN-expression of keratinocytes induced by IFN-γ, IL-6 and IL-22 but not by TGF-β1.

Conclusion

These results indicate that TGF-β1, IFN-γ, IL-6, and IL-22 induce PDPN-expression of keratinocytes, which might be significantly involved in the wound healing process as well as in the pathomechanism of hyperproliferative psoriatic epidermis.     

女性无症状淋病患者胸腺基质淋巴细胞生成素的表达及与IL-17,IL-10关系

目的探讨女性无症状淋病患者中胸腺基质淋巴细胞生成素(TSLP)的表达及其与IL-17,IL-10水平的关系。方法选择123例女性无明显症状淋病患者为无明显症状组,32例有症状女性淋病患者为有症状组,放射免疫法(RIA)测定血清孕酮浓度;荧光定量PCR和酶联免疫吸附法(ELISA)在mRNA水平和蛋白水平检测宫颈分泌物中TSLP,IL-17和IL-10的水平。结果女性无明显症状淋病患者中TSLP表达升高,其表达与孕激素水平及IL-10呈显著正相关(r=0.99,0.97,P均0.01),与IL-17呈显著负相关(r=-0.89,P0.01)。有症状组和正常对照组TSLP和IL-10水平差异无统计学意义(P均0.05)。有症状组IL-17水平明显高于正常对照组,差异有统计学意义(P0.01)。结论孕激素可能通过上调TSLP表达在女性无症状淋球菌感染中发挥作用。     

蒽林在体外能抑制人单核细胞分泌IL-6、IL-8和TNF-α,但不影响IL-1的分泌

蒽林是使用最广泛的银屑病局部治疗药物。在大量研究证明蒽林是安全和有效的同时,其作用模式仍未完全搞清。除了对角朊细