斑秃患者外周血CD4+CD25+Foxp3调节性T细胞及T淋巴细胞亚群的测定

目的 研究斑秃患者外周血中CD4+CD25+调节性T细胞数量及CD4+、CD8+ T淋巴细胞亚群数量与斑秃疾病严重程度的关系。方法 对斑秃进行病情分组，以流式细胞仪检测17例重度、15例局限型斑秃患者和25例正常人对照者外周血中有功能活性的CD4+CD25+调节性T细胞（即CD4+CD25+ Foxp 3 T 细胞）在CD4+ T淋巴细胞中的比率，CD4+和CD8+占T淋巴细胞的比率。 结果 重度斑秃患者外周血中有功能活性的CD4+CD25+ Foxp 3 T细胞占CD4+ T细胞比率为0.54% ± 0.31%，显著低于正常人对照组（3.21% ± 0.76%）及局限型斑秃患者（2.71% ± 0.37%，P ＜ 0.001）；与正常人对照组比较，差异无统计学意义（P ＞ 0.05）。重度斑秃患者的CD4+占T淋巴细胞的比率为32.61% ± 3.48%，显著低于正常人对照组（43.0% ± 3.63%，P ＜ 0.001），而CD8+占T淋巴细胞的比率为40.96% ± 8.54%，显著高于正常人对照组（25.23% ± 2.14%，P ＜ 0.001）。局限型斑秃患者的此两项指标分别为41.25% ± 4.27%和26.6% ± 2.28%，与对照组差异无统计学意义（P ＞ 0.05）。重度斑秃患者的CD8+占T淋巴细胞的比率与CD4+CD25+ Foxp 3调节性 T 细胞占CD4+ T细胞的比率有负相关关系（r ＝ －0.94，P ＜ 0.001）。结论 重度斑秃可能与外周血中CD4+CD25+ T细胞数量的减少和功能活性的降低有关。     

毛囊免疫赦免与斑秃

近年来研究证实生长期毛囊为免疫赦免部位 ,生长期毛球主要组织相容性复合体Ⅰ分子表达呈阴性。斑秃主要累及生长期毛囊 ,以毛囊周围淋巴细胞浸润和毛囊上皮细胞异常表达主要组织相容性复合体Ⅰ和Ⅱ分子为特征。因此 ,目前认为斑秃发病与生长期毛囊丧失免疫赦免地位有关     

斑秃毛囊退行性变及局部炎症细胞浸润的研究进展

斑秃是一种非瘢痕性的炎症性脱发性疾病,病情多能自限,但容易复发。斑秃发病机制不明,组织病理上表现为生长期毛囊周围炎症浸润及毛囊退行性变两个部分。目前研究认为,内外源因素作用于遗传易感人群引起生长期毛囊深层周围炎症细胞浸润,浸润的炎症细胞及细胞因子、神经肽等形成恶性循环,循环结局为毛囊上皮细胞凋亡,大批毛囊同时陕速进入退行期,导致斑秃发生。     

斑秃患者外周血T淋巴细胞亚群及CD4~+CD25~+调节T细胞的检测

目的检测斑秃(AA)患者外周血T淋巴细胞亚群及CD4+CD25+调节性T(Tr)细胞数量变化,分析AA的可能病因。方法利用流式细胞仪和单克隆荧光抗体技术,测定重度和局限性AA各40例患者外周血中T淋巴细胞亚群占T淋巴细胞的比率及CD4+CD25+Tr细胞在CD3+CD4+T淋巴细胞中的比率。结果重度AA患者外周血中CD4+CD25+Tr细胞占CD3+CD4+T细胞的比率为(1.43±0.74)%,显著低于正常对照组(2.25±0.97)%(P<0.01),重度AA患者的CD4+T占T淋巴细胞的比率为(31.42±6.66)%,略高于正常对照组(30.69±7.47)%(P>0.05),差异无显著性,而CD8+T占T淋巴细胞的比率为(25.86±4.35)%,明显高于正常对照组(22.42±6.10)%(P<0.01);局限性AA患者的三项指标分别为(2.14±0.87)%,(32.60±10.27)%和(21.59±5.24)%,与对照组差异无显著性(P>0.05)。结论AA患者外周血中CD4+CD25+Tr明显低于正常对照组,CD8+T比率明显高于正常对照组,可能是导致重度AA发病的主要免疫机制。     

系统性红斑狼疮患者淋巴细胞CD126 的表达

我们分别采用流式细胞仪结合微量全血双标记免疫荧光法和半定量逆转录聚合酶链反应 (RT-PCR)技术检测了 33例 SLE患者 CD3＋与 CD19＋淋巴细胞表面 CD126表达水平和外周血单一核细胞 (PBMC)内 CD126 mRNA表达水平,现报道如下。 一、材料与方法 (一 )研究对象：符合 1982年美国风湿病协会修订的 SLE诊断标准的患者共 33例,男 6例,女 27例,年龄 17～ 53岁,平均年龄 (32.2± 10.1)岁。参照文献 [1]按受检时的临床表现及实验室检查结果对 SLE疾病活动性（ SLEDAI）进行评分,受检时总分 >9分者判为活动期, 18例,男 3例,女…     

紫外线照射对银屑病患者淋巴细胞CD44及CD54分子表达的影响

目的：进一步了解紫外线照射（UVR）对银屑病患者系统免疫的影响,方法：采用流式细胞仪对UVR治疗前后银屑病患者淋巴细胞CD44及CD54的表达进行研究。结果：（1）银屑病患者CD44及CD54表达量较对照组显著增高（P均＜0．001）,（2）UVR治疗后患者CD44及CD54表达量显著降低（P＜0．001,P＜0．05）,（3）停止治疗半月后,患者CD44及CD54表达量接近治疗前水平,结论：UVR治疗银屑病可能与其减少淋巴细胞粘附分子表达有关。     

斑秃毛囊免疫赦免机制的进展

近年来大量研究显示,生长期毛囊也是免疫赦免器官之一。有学者提出,斑秃毛囊免疫赦免消失导致斑秃发生。其中一些炎症因子在免疫赦免丧失及重建过程中起到关键作用。而黑素细胞相关肽在发病机制中可能就是自身抗原。     

斑秃患者皮损中CD4+和CD8+T细胞的检测

斑秃病因未明．细胞免疫可能参与了斑秃的发病．CD4^ 和CD8^ T细胞是两种重要的免疫细胞，在免疫调节中起重要作用。为了研究这两种细胞在斑秃发病中的作用．笔者采用免疫组化的方法对斑秃应损和正常头皮中CD4^ 和CD8^ T细胞的分布情况进行了检测．现报告如下。     

Receptor site dominance after hair transplantation in alopecia areata

A 32-year-old woman presented with a patchy and ophiasis type of alopecia areata. She reported that at the age of 25 she had undergone plastic surgery for the same hair problem. In the occipital region, partial excision of bald areas and transplantation of punched grafts from unaffected areas of her scalp had been performed, but these grafts completely lost their hair shortly after transplantation. At the age of 30 she had developed, in addition, patchy alopecia areata in other areas of the scalp. The present observation of receptor site dominance of the area affected by alopecia areata suggests that the primary abnormality is situated in the affected tissue, and that the disease is caused by local spreading of a hitherto unknown factor.     

斑秃患者皮损丝聚蛋白的表达

【摘要】 目的 探讨丝聚蛋白表达水平与斑秃患者特应性素质和疾病严重程度的关系。方法 分析37例斑秃患者的临床资料及实验室资料,取斑秃皮损和正常对照的头皮进行免疫组化染色,用荧光半定量RT-PCR检测22例斑秃皮损和正常对照的头皮丝聚蛋白在蛋白质和信使RNA的表达水平。结果 斑秃皮损丝聚蛋白和其mRNA的表达水平较正常对照明显降低（P < 0.05或0.01）,而且这种降低在脱发面积较大、病程较长和有指甲改变的斑秃患者中更明显,但降低水平与是否伴发特应性疾病无关。斑秃患者伴特应性疾病组与不伴特应性疾病组之间性别、发病年龄、病程、脱发面积、家族史、甲改变、血清IgE和嗜酸粒细胞升高的发生率等方面差异均无统计学意义。结论 斑秃患者其皮损丝聚蛋白及其mRNA的表达水平均降低,提示丝聚蛋白可能参与斑秃的发病,并和疾病的严重程度有关。     

神经肽和HPA轴因素在斑秃发病中的作用

斑秃是一种毛囊的自身免疫性疾病,其发病机制中精神应激机制的研究热点集中在两方面:一是对作为大脑-皮肤之间的神经免疫内分泌联系的神经肽类的研究:外部应激因素可通过P物质、降钙素基因相关肽、神经生长因子、肥大细胞、巨噬细胞、γ8T细胞组成相互作用的网络,这些物质组成"脑-毛囊轴",毛囊对这些应激介质高度敏感,应激正是通过这个途径影响毛发生长;二是对皮肤作为外周类似下丘脑-垂体-肾上腺轴功能单位的研究:皮肤具有自己的神经内分泌系统,皮肤及其附属器也能产生同样的系统性应激反应所需要的介质,人类皮肤也可表达促皮质素释放激素.     

Expression of beta-catenin,p63 and CD34 in hair follicles during the course of androgenetic alopecia

During the hair growth cycle, the hair follicle appears to recapitulate part of its embryogenesis where both beta-catenin and p63 participate. The aim of the present study was to investigate the hypothesis that beta-catenin and p63 protein may be involved in the pathogenesis of androgenetic alopecia. Second, expression of CD34 protein was used to assess the capillary density of the affected skin. Cadavers were used as samples and the results showed that analysis of beta-catenin, p63 and CD34 expressions in human cadaverous scalp skin by immunohistochemical techniques were possible. We detected a higher expression of p63 in occipital skin in comparison to the affected frontal areas. However, we found only minimal changes in beta-catenin expression comparing frontal and occipital areas. A completely new finding was the expression of CD34 positive cells in the outer root sheath of hair follicles.     

Cytokines and growth factors influence hair growth in vitro. Possible implications for the pathogenesis and treatment of alopecia areata

Factors that influence the growth of the anagen hair follicle or initiate the switch to a catagen growth pattern have so far not been definitely determined, but there is increasing evidence that cytokines and growth factors play an important role during these processes. Recently we detected an aberrant in situ expression pattern of cytokines of the Th1 type (IFNγ, IL-2) plus IL-1β expression in untreated alopecia areata (AA), and a switch to high levels of IL-10 TGF-β1 expression after successful treatment with the contact allergen diphenylcyclopropenone (DCP). Hence the question arose as to whether cytokines are able to arrest hair growth and whether IL-10 or TGFβ1 have the capacity to antagonize this process. Using whole-organ cultures of microdissected human hair follicles we studied the effect of a panel of cytokines and growth factors on hair growth and on the gross morphology of the hair follicles in vitro. IL-2, IL-10 and IFN-γ had no effect in this regard, whereas TGFβ1 partially inhibited hair growth and EGF, TNFα and IL-1β completely abrogated it. EGF and TNFα induced the formation of a club-like hair follicle, similar to catagen morphology of the hair bulb, whereas hair follicles grown in the presence of IL-1β or TGFβ1 showed no particular morphological changes. We conclude that cytokines and growth factors are pivotal regulators of hair growth at least in vitro. IL-1 is suggested as playing an important role during the pathogenesis of AA. Possible mediators of therapeutic contact dermatitis (IL-10, TGFβ1, TNFα, PGE₂) are, at least in vitro, not able to antagonize the IL-1β-triggered hair growth inhibition. Therefore, we infer that these mediators rather ‘modulate’ the immune response in AA.     

Altered polyamine profiling in the hair of patients with androgenic alopecia and alopecia areata

Hair follicles are among the most highly proliferative tissues. Polyamines are associated with proliferation, and several polyamines including spermidine and spermine play anti‐inflammatory roles. Androgenic alopecia results from increased dihydrotestosterone metabolism, and alopecia areata is an autoimmune disease. This study aimed to investigate differences in polyamine profiles in hair samples between patients with androgenic alopecia and alopecia areata. Polyamine concentrations were determined through high‐performance liquid chromatography‐mass spectrometry. Hair samples were derivatized with isobutyl chloroformate. Differences in polyamine levels were observed between androgenic alopecia and alopecia areata compared with normal controls. In particular, polyamine levels were higher in alopecia areata patients than in normal controls. Certain polyamines displayed different concentrations between the androgenic alopecia and alopecia areata groups, suggesting that some polyamines, particularly N‐acetyl putrescine (P = 0.007) and N‐acetyl cadaverine (P = 0.0021), are significantly different in androgenic alopecia. Furthermore, spermidine (P = 0.021) was significantly different in alopecia areata. Our findings suggest that non‐invasive quantification of hair polyamines may help distinguish between androgenic alopecia and alopecia areata. Our study provides novel insights into physiological alterations in patients with androgenic alopecia and those with alopecia areata and reveals some differences in polyamine levels in hair loss diseases with two different modes of action.