16例急性移植物抗宿主病临床资料分析

对16例急性移植物抗宿主病（GVHD）患者进行回顾总结：患者皮疹多级为I级-II级，以斑疹为主，6例有胃肠道症状，其中2例有肝脏受累。作者对皮疹发生时间、部位及胃肠道症状进行分析，认为GVHD的发生及其程度直接影响到移植病人的预后，而皮疹则是GVHD的一个重要标志。     

芳维A酸氨丁三醇与活性维生素D3对HaCaT细胞中相关受体表达的影响

目的探讨芳维A酸氨丁三醇(AT)与1,25-二羟基维生素D3[1,25-(OH)2D3]单用或联合应用对RXRα及VDR表达的影响。方法培养HaCaT细胞至对数生长期,分为AT,AT与1,25-(OH)2D3联合,1,25-(OH)2D3及空白对照组,避光孵育48h,提取RNA,两种PCR法检测RXRα,VDR的基础表达及各组RXRα,VDR在转录水平的表达变化。结果HaCaT细胞中RXRα,VDR自然表达,RXRα含量明显高于VDR,约为其7倍;单用1,25-(OH)2D3组中VDR转录水平明显上调约8倍,其余组的VDR,RXRα表达与对照组相比差异无显著性。结论HaCaT细胞中RXRα含量明显高于VDR,单用1,25-(OH)2D3可明显上调VDR转录水平,而联合AT后VDR基本恢复正常,AT可能通过影响RXR/VDR异二聚体对1,25-(OH)2D3信号传导途径产生影响。     

维A酸对银屑病患者外周血T淋巴细胞增殖及JAK3表达的影响

目的探讨第三代维A酸(芳维A酸氨丁三醇)和第二代维A酸(依曲替酸)对银屑病患者T淋巴细胞增殖的影响及其机制。方法抽取银屑病患者外周血,分离T淋巴细胞,经不同浓度药物处理后,台盼蓝染色检测细胞活力,用改良MTT法检测淋巴细胞的增殖能力;分别用Real-time PCR和蛋白印迹方法检测JAK3,STAT5的mRNA和蛋白表达水平。结果芳维A酸氨丁三醇与依曲替酸在10-9~10-6浓度范围内,均对银屑病患者外周血T淋巴细胞的增殖有抑制作用,且呈剂量依赖性,芳维A酸氨丁三醇比依曲替酸抑制作用更明显;两种药物均可下调银屑病患者T淋巴细胞JAK3基因的表达,且芳维A酸氨丁三醇的下调作用更显著,但STAT5蛋白表达无变化。结论芳维A酸氨丁三醇和依曲替酸可明显抑制银屑病患者外周血T淋巴细胞的增殖,其机制可能与下调JAK3表达有关。     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

Effects of α-melanocyte-stimulating hormone on the production of TNF-α and IL-10 by peripheral blood mononuclear cells from patients with psoriasis

Objective To investigate the effects of alpha-melanocyte-stimulating hormone (alpha-MSH) on the production of tumor necrosis factor-alpha (TNF-alpha) and intedeukin-10 (IL-10) by peri-pheral blood monohuclear cells (PBMCs) from patients with psoriasis vulgaris. Methods Heparinized peri-pheral blood was obtained from 20 patients with psoriasis vulgaris and 10 healthy human controls. PBMCs were isolated, cultured in complete medium, and stimulated with phytohemagglutinin (PHA) alone, the com-bination of PHA and various concentrations of alpha-MSH, or nothing. After another 48-hour culture, ELISA and real-time PCR were performed to measure the secretion levels of TNF-alpha and IL-10 in the super-natants of cultured PBMCs as well as the mRNA expression levels of TNF-alpha and IL-10 in PBMCs. Results The secretion level of TNF-alpha in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone was significantly higher than that from normal control-derived PBMCs (329.87 ± 99.33 ng/L vs 116.95 ± 37.15 ng/L, 1756.01 ± 183.60 ng/L vs 1287.30 ± 152.36 ng/L, both P<0.01). alpha-MSH of all tested concentrations (10-13, 10-11, 10-7,mol/L) could inhibit the secretion of TNF-alpha by PBMCs com-pared with PHA alone (all P < 0.01), and the maximum effective concentration was 10-13 mol/L. On the con-Wary, a significant decrease was observed in the secretion level of IL-10 in the supematants of patient-derived PBMCs stimulated by nothing or PHA alone compared with normal control-derived PBMCs (P <0.05 or 0.01). Moreover, the secretion of IL-10 by PBMCs was promoted by alpha-MSH of all tested con-centrations (P < 0.01 or 0.05), with the maximum effective concentration being 10-13 mol/L (P < 0.01). The alpha-MSH of 10-13 mol/L down-regulated the mRNA expression of TNF-alpha (P < 0.001), but up-regnlated that of IL-10 (P < 0.001) in PHA-stimulated PBMCs from patients. Conclusion alpha-MSH can regulate the production of TNF-alpha and IL-10 by PHA-stimulated PBMCs from patients with psoriasis vulgaris.     

维A酸对砷刺激角质形成细胞增殖的拮抗作用

目的研究维A酸药物对三价砷刺激角质形成细胞增殖的拮抗作用及其机制。方法以体外培养的角质形成细胞为对象,低浓度三价砷预处理细胞刺激增殖,并用3H-TdR掺入法分析不同维A酸药物对细胞增殖的拮抗效应,进一步用流式细胞仪检测细胞周期变化。结果一定浓度三价砷可刺激角质形成细胞增殖,加入不同浓度芳维A酸氨丁三醇、依曲替酸处理24h,显示0.01~1μmol/L维A酸可不同程度拮抗砷剂的刺激增殖效应,芳维A酸氨丁三醇作用强于依曲替酸。流式细胞仪检测细胞周期分布变化,显示维A酸处理后S期细胞比例降低,G0-G1期细胞比例升高。结论低浓度的三价砷可刺激角质形成细胞增殖,而维A酸可拮抗砷剂的刺激增殖作用,使S期细胞比例降低,可能是维A酸类药物治疗砷相关皮肤病的机制之一。     

特发性CD4+T淋巴细胞减少症研究进展

特发性CD4 T淋巴细胞减少症又称人类免疫缺陷病毒阴性艾滋病样综合征。患者主要特点为CD4 T淋巴细胞减少 ,具有与艾滋病相似的临床表现 ,但又无人类免疫缺陷病毒感染的证据。发病机制主要与T淋巴细胞增生异常、凋亡增强及表面受体功能改变有关。除积极治疗各种机会感染外 ,最根本的治疗是重建免疫功能     

银屑病并发常见皮肤恶性肿瘤的研究现状

银屑病是一种免疫介导的慢性炎症性疾病，常伴有冠心病、糖尿病、高血脂、高尿酸血症等共病。研究显示银屑病患者伴发皮肤恶性肿瘤风险升高，以鳞状细胞癌为主，而基底细胞癌和黑素瘤等风险相对较低。通过对其并发皮肤恶性肿瘤的危险因素分析发现：既可以与银屑病患者的慢性炎症状态相关，也可能和银屑病的部分治疗方式相关，如光疗、甲氨蝶呤、肿瘤坏死因子抑制剂等对机体具有一定的诱导基因突变或免疫抑制的功能。本文对近年来银屑病患者合并各类皮肤肿瘤的现状、病因和发病机制进行了阐述，并探讨其防治策略。     

环状肉芽肿病因及发病机制

环状肉芽肿是一种以环状丘疹或结节性损害为特征的慢性皮肤病，目前病因和发病机制尚不明确。一般认为是机体对病毒感染、外伤、日晒或糖尿病、甲状腺炎相关免疫性疾病、疫苗接种、恶性肿瘤等异常免疫状态下的肉芽肿反应。对上述几个方面的涉及病因、发病机制的研究报告进行了综述。     

痤疮及非痤疮患者皮脂腺内的雄激素代谢

为确定寻常痤疮患者皮脂腺 (ＳＧ)内是否因雄激素产生增多而导致皮脂分泌增加 ,作者测定了不同性别的痤疮和非痤疮患者ＳＧ中1 7β 羟类固醇脱氢酶 (1 7β ＨＳＤ)和 5α 还原酶(5α Ｒ)的活性、血清雄激素水平 ,并比较血清雄激素与组织中以上酶类的活性关系。 3 4例 1 8～ 3 4岁的研究对象中 ,男女痤疮患者各 8例 ,无痤疮者中 ,男 8例 ,女 1 0例。测定结果 :无论在男性或女性中 ,前额皮肤的ＳＧ中 5α Ｒ和1 7β ＨＳＤ活性在有痤疮与无痤疮者间差异无显著性。男性 1 7β ＨＳＤ和 5α Ｒ活性显著高于女性 ,男性 1 7β ＨＳＤ氧化活性比女…