Imbalance of T‐helper 17 and regulatory T cells in patients with alopecia areata

There is mounting evidence that T helper (Th)17 cells and regulatory T cells (Treg) play parts in the pathogenesis of autoimmune disease. Hence, levels of these T‐cell subsets in patients with alopecia areata (AA) merit investigation. Our goal was to assess Th17 and Treg levels in peripheral blood mononuclear cells (PBMC) and scalp lesions of patients with AA, correlating the findings with clinical characteristics. PBMC of 177 patients with AA (test group) and 42 healthy controls and scalp tissues of 33 patients and 15 healthy controls were collected. Levels of Th17 and Treg subsets were then determined via flow cytometry and immunohistochemical staining, correlating results in test subjects with clinical features of AA. Th17 levels were significantly higher in patients, whereas Treg levels were lower by comparison. Furthermore, Th17 levels in patients with disease of short duration or in the active phase were significantly higher, relative to their respective counterparts. Th17 levels also negatively correlated with disease duration. While Treg levels were higher in severe AA than in mild AA. Results of lesions were parallel to findings of PBMC. Our data indicates an imbalance in the immune state of patients with AA.     

The role of cytokines and chemokines in the T‐cell‐mediated autoimmune process in alopecia areata

The aetiology of alopecia areata (AA) is still not fully understood. However, recent clinical and experimental studies have provided insights into the pathomechanisms of AA and revealed that it is an organ‐specific and cell‐mediated autoimmune disease. Some triggers, such as viral infections, trauma, hormones and emotional/physical stressors, may cause activation of autoreactive T cells that target hair follicle (HF) autoantigens. In these immunological responses, cytokines and chemokines are regarded as key players that mediate the autoimmune inflammation. This results in the collapse of HF immune privilege, which is central to the pathogenesis of AA. This essay will focus on how cytokines and chemokines contribute to the immunological aspects of AA. The management of AA often remains difficult in a number of cases. Our review suggests that novel therapies for AA may involve targeting cytokines and chemokines.     

斑秃患者外周血T细胞亚群的测定

斑秃是皮肤科的常见疾病，但病因不明，发病机理不确切。目前多认为它是一种与免疫有关的疾病犤１，２犦。为了进一步探讨斑秃的病因和发病机理，我们运用免疫荧光流式细胞术测定３０例斑秃患者外周血的T细胞亚群，并对其在斑秃发病中的意义进行了探讨。１临床资料：选择我科斑秃患者３０例，均未使用过皮质类固醇或免疫抑制剂，并具备斑秃的典型临床表现。其中，男性１６例，女性１４例；年龄１７～５４岁，平均３４．６岁；其中稳定期１３例，活动期１７例；病程２天到１年，平均３．４个月。均为局限型病例，皮损数目２到７个不等，平均…     

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;     

Regulatory T‐cell cytokines in patients with nonsegmental vitiligo

In the etiopathogenesis of vitiligo, the role of suppressor cytokines, such as transforming growth factor‐β (TGF‐β) and interleukin‐10 (IL‐10), associated with regulatory T‐cells (Treg) is not completely known. In this study, the role of Treg‐cell functions in the skin of patients with nonsegmental vitiligo was investigated. Lesional and nonlesional skin samples from 30 adult volunteers ranging in age from 18 to 36 years with nonsegmental vitiligo were compared with normal skin area excision specimens of 30 benign melanocytic nevus cases as controls. All samples were evaluated staining for forkhead box P3 (Foxp3), TGF‐β, and IL‐10 using the standardized streptavidin–biotin immunoperoxidase immunohistochemistry method. Foxp3 expression was lower in lesional vitiligo skin specimens compared to controls; it was also lower in lesional vitiligo specimens than nonlesional vitiligo specimens. IL‐10 levels were lower in lesional vitiligo specimens compared to the controls, whereas IL‐10 expression was significantly lower in lesional specimens compared with nonlesional specimens. TGF‐β expression was higher in both lesional and nonlesional skin specimens of patients with vitiligo compared to controls. TGF‐β expression was lower in lesional skin specimens than nonlesional skin specimens. In addition, there was no significant correlation between Foxp3 expression with TGF‐β and IL‐10 expressions in lesional skin specimens in the vitiligo group. In this study, results supporting the contribution of Treg cells and IL‐10 deficiency to the autoimmune process were obtained. Therefore, future studies are necessary to demonstrate the definitive role of Treg‐cell functions in the etiopathogenesis of vitiligo.     

斑秃患者外周血白细胞介素35的表达及其对调节性T细胞的功能调控

目的:观察斑秃患者外周血白细胞介素35（IL-35）表达变化,评估IL-35对斑秃患者调节性T细胞（Treg）活性的调控。方法:收集2019年12月至2021年1月在山西省人民医院就诊的斑秃患者81例（斑秃组）和健康志愿者27例（对照组）,分离血清和外周血单个核细胞（PBMC）,酶联免疫吸附试验（ELISA）检测血清I...     

Th22及其细胞因子在斑秃患者外周血的表达和意义

目的：探讨Th22及其细胞因子在斑秃患者外周血中的表达及其临床意义,分析T淋巴细胞在斑秃发病机制中的作用。方法选取上海市闵行区中心医院2015年1月至2016年5月收治的38例斑秃患者作为研究对象,设为斑秃组;同时取同期健康体检38例作为健康对照组,用流式细胞仪检测Th22细胞水平,用酶联免疫吸附检测血清中IL?22、IL?17的水平。结果斑秃组外周血Th22、Th17、IL?17+IL?22+CD4+、IFN?γ+IL?22+CD4+T细胞表达水平均高于健康对照组（P<0.01）。斑秃组血清IL?22、IL?17水平均高于健康对照组（P<0.05）;与轻型斑秃患者和稳定期患者相比,重型斑秃和活动期患者Th22、Th17、IL?17+IL?22+CD4+、IFN?γ+IL?22+CD4+T细胞及血清IL?22、IL?17的表达进一步升高（P<0.05）。结论 Th22及其细胞因子可能参与斑秃的发生、发展、预后。     

斑秃发病机制中相关因子的研究进展

斑秃是生长期毛囊自身免疫性疾病,受内源性或外源性因素的刺激诱发.研究显示,在斑秃发病过程中,细胞因子和一些小分子起关键作用.干扰素-γ、白介素类以及肿瘤坏死因子-α是疾病中常见的重要细胞因子.干扰素-γ诱导的单核因子,干扰素诱导蛋白10,B细胞激活因子,HLA抗原以及应激激素在斑秃中起一定作用.概述斑秃病因的复杂性以及潜在的机制,提出可能的治疗方法.

Abstract：

Alopecia areata (AA) is an autoimmune disease affecting the anagen-stage hair follicles, and is triggered by internal or external factors. It has been revealed that cytokines and some small molecules play essential roles in the development of AA. Interferon (IFN)-γ, interleukins and tumor necrosis factor-α are common cytokines involved in the pathogenesis of diseases. Monokine induced by IFN-'γ, IFN-γ inducible protein 10, B cell activating factor, HLA antigens, as well as stress hormones play certain roles in the development of AA. Within the scope of this paper, the authors attempt to summarize the complexity of etiology of, underlying mechanisms of and possible treatment options for AA.     

Clear association between serum levels of adipokines and T‐helper 17‐related cytokines in patients with psoriasis

Background. Psoriasis represents one of the T‐helper (Th)17‐mediated autoimmune diseases, and has been shown to be associated with metabolic syndrome (MetS). It has been reported that some adipokines and Th17‐related cytokines are altered in patients with psoriasis. Aim. To examine the relationship between levels of adipokines and Th17‐related cytokines in the serum of patients with psoriasis compared with healthy controls. Methods. We enrolled 30 patients with psoriasis and 30 normal controls in the study, and used ELISA to measure serum adipokines and Th17‐related cytokines. The association between each adipokine and each cytokine was determined using Pearson correlation analysis. Multiple regression analysis using all adipokines and Th17‐related cytokines as covariates was also performed. Results. Pearson correlation analysis showed a strong positive association between chemerin and resistin levels and between adiponectin and high molecular weight adiponectin in normal controls. By contrast, in patients with psoriasis, resistin levels were significantly positively associated with tumour necrosis factor‐α, while there was a strong negative association between retinol binding protein‐4 and interleukin (IL)‐6 levels. Interestingly, a marked positive correlation between IL‐22 and adiponectin was also found in patients with psoriasis. Leptin levels correlated positively with IL‐6 in patients with psoriasis, but this did not reach significance. The correlations identified by the multiple regression analyses were almost identical to those from the Pearson analyses. Conclusions. These data suggest that distinct interaction between adipokines and Th17 cytokines is involved in the pathogenesis of psoriasis.     

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。     

Primary cutaneous follicular helper T‐cell lymphoma

Follicular helper T‐cells (TFH) represent a specific subset of CD4‐positive helper T‐cells that help B‐cells to differentiate into long‐lived antibody‐secreting plasma cells or memory B‐cells. The expression of TFH markers in neoplastic T‐cells, traditionally related to the angioimmunoblastic (AITL) subgroup of peripheral T‐cell lymphomas, is nowadays well‐known to be more widespread than previously thought. We report hereby a case of cutaneous T‐cell lymphoma in a 75‐year‐old woman, whose morphological and immunophenotypical features raises the differential diagnosis between cutaneous involvement by AITL and the recently described primary cutaneous T‐cell lymphoma with follicular helper‐phenotype.     

Selective changes in lymphocytic differentiation antigens in the peripheral blood of patients with alopecia areata treated with oral zinc

Recent research has shown that the regrowth of hair in alopecia areata (AA) is associated with the normalization of the CD4+/CD8+ ratio, which is usually in an unbalanced state. This dysbalance is represented by an increased level of CD4+ and a decrease of CD8+ cells and found not only in the bulbar region but also in the peripheral blood. Since zinc generally acts as a polyclonal T-cell activator and has been proved a useful oral therapeutic in AA, we additionally controlled the levels of CD4+ and CD8+ cells as well as other lymphocyte subpopulations in the peripheral blood of AA patients before and during oral treatment with zinc. Our data revealed a significant raise of CD3+, CD8+, CD19+, HLA-DQ+, HLA-DR+, and Leu 2a+8+ cells during oral therapy with zinc. We conclude that the successful treatment of AA with zinc may be due to immunomodulation, especially through the increase of CD8+ cells.