生殖器疱疹患者外周血淋巴细胞表型表达水平的研究

目的:检测生殖器疱疹患者(GH)外周血T淋巴细胞亚群、NK细胞和B细胞的表达水平,探讨其复发机制与细胞免疫功能之间的关系。方法:应用流式细胞仪检测60例复发性生殖器疱疹患者(RGH)外周血T淋巴细胞亚群、NK细胞和B细胞的表达水平,并与20名初发生殖器疱疹患者、35名健康对照者外周血检测结果相比较。结果:①复发组与对照组相比,外周血中T细胞、CD4 细胞、NK细胞所占比例,以及CD4 /CD8 均降低,差异有统计学意义;CD8 细胞百分比升高,差异有统计学意义;B细胞比例差异无统计学意义。②初发患者和对照组相比,除NK细胞降低有统计学意义外,其它差异无统计学意义。③复发组与初发组相比,复发组T细胞、CD4 细胞、CD4 /CD8 均降低,CD8 细胞百分比升高,差异有统计学意义;B细胞、NK细胞比例差异无统计学意义。结论:生殖器疱疹复发可能与患者细胞免疫功能紊乱有关。     

阿维A联合重组人白介素-2对尖锐湿疣患者T淋巴细胞亚群及复发的影响

目的观察阿维A联合重组人白介素-2对尖锐湿疣(CA)患者外周血T淋巴细胞亚群的影响及预防复发的效果。方法入选患者随机分为两组,A组30例用微波彻底清除疣体后应用重组人白介素-2注射液20万U肌注,隔日1次,连用7次;B组34例采用微波彻底清除疣体后联合阿维A及重组人白介素-2治疗。所有患者均随访6个月。治疗前及治疗后8周抽取外周血检测T淋巴细胞亚群,并与25例健康对照组进行比较。结果治疗前CA患者与健康对照组比较,CD4+细胞百分比、CD4+/CD8+比值降低,差异有统计学意义(P<0.05),CD8+细胞百分比升高,差异亦有统计学意义(P<0.05),CD3+细胞百分比无明显变化;治疗后A,B组CD4+细胞百分比及CD4+/CD8+比值明显升高,CD8+细胞百分比降低,与治疗前相比差异均有统计学意义(P均<0.05),CD3+细胞无明显变化;治疗后A组,B组比较,A组CD4+细胞百分比、CD8+细胞百分比、CD4+/CD8+比值变化明显小于B组,差异有统计学意义(P<0.05);治疗后A组CD4+细胞百分比、CD4+/CD8+比值仍低于对照健康组,差异有统计学意义(P<0.05),治疗后B组与健康对照组相比上述指标差异无统计学意义(P>0.05)。A组复发率33.33%,明显高于B组的11.76%(P<0.05)。结论 CA患者存在细胞免疫功能异常,阿维A与重组人白介素-2可调节CA患者外周血T淋巴细胞亚群,从而调节患者细胞免疫功能;两者联合应用治疗CA可获得较好疗效,并能降低其复发率。     

UVB致小鼠皮肤癌变中Fas/FasL,CD4及CD8的表达

目的通过窄谱中波紫外线(NB-UVB)照射诱发小鼠皮肤肿瘤,探讨Fas/FasL,CD4及CD8在Bowen病(BD)、光老化皮肤及正常小鼠皮肤中的表达情况,加深对皮肤肿瘤Fas/FasL凋亡途径和免疫逃逸机制及周围浸润淋巴细胞类型的认识。方法将42只健康的昆明种小鼠分为两组,慢性照光组(UVB)32只,正常组10只。应用免疫组化法检测其Fas/FasL,CD4及CD8的表达情况。结果成功制作了NB-UVB致小鼠皮肤癌模型。Fas表达光老化皮肤组高于正常鼠皮肤,BD组低于光老化组,FasL表达BD组和光老化组均高于正常鼠皮肤,BD组较光老化组增高,CD4在BD组较正常鼠皮肤及光老化皮肤组均降低,光老化组较正常鼠增高,CD8在BD组、光老化组较正常鼠增高,差异均有统计学意义(P均<0.05),而BD组和光老化组间差异无统计学意义(P>0.05)。结论 FasL在光老化皮肤中表达增高,在BD中进一步增高,支持了Fas/FasL系统启动细胞凋亡过程和肿瘤细胞通过表达FasL来逃避机体免疫监视的学说。BD组与正常皮肤组相比,CD4表达降低,CD8表达增高,这可能与BD是表皮内鳞状细胞癌且存在向侵袭性癌转变的倾向有关。     

某些细胞因子在天疱疮皮损中的表达

目的:检测Th2类细胞因子在天疱疮皮损中的表达.方法: 选用单克隆抗体CD4,CD8,CD25,CD54和CD124等,对40例天疱疮患者的皮损及皮损周围皮肤标本用S-P法进行免疫组化研究,同时以20例正常人皮肤组织为对照.结果: CD4+和CD8+的T细胞见于全部标本真皮浸润的单一核细胞内,且以CD4+的T细胞为主(P<0.01),在表皮CD8+的T细胞在寻常型天疱疮和红斑型天疱疮比较有显著性差异(P<0.01),27例病人显示CD25染色阳性,与皮损周围相比CD54在皮损处表达增多(P<0.05).某些CD124阳性细胞见于表皮及真皮.对照组中CD4+和CD8+T细胞稀少,CD4/CD8比值为1.4,在皮损及皮损周围的皮肤中CD25的表达无显著性差异(P>0.05),而角质形成细胞不表达CD25.CD54的表达见于血管内皮细胞和真皮血管周围的单一核细胞,与皮损周围相比,皮损处CD54+增加(P<0.05).结论:细胞免疫在天疱疮的发病中有重要作用.     

慢性荨麻疹患者外周血CD4+CD25+调节性T细胞的表达

目的:探索调节性T细胞(regulatory T cells,Tregs)在慢性荨麻疹(CU)发病中的作用.方法:采用流式细胞术分别检测CU患者和健康人外周血CD3+、CD4+、CD8+、CD4+CD25+T细胞的表达水平.结果:与健康对照组比较,CU患者外周血CD3+T细胞比例无明显变化,CD4+T细胞增高(P ＜ 0.05),CD4+CD25+T细胞表达水平显著增高(P ＜ 0.01),CD8+T细胞数量降低(P ＜ 0.05),CD4+/ CD8+比值明显升高(P ＜ 0.05).自身血清皮肤试验(ASST)阳性组与阴性组的CU患者CD4+CD25+Tregs 细胞的数量无统计学差异.结论:CU患者外周血存在Treg细胞及其他T淋巴细胞亚群的数量异常和分化失衡,这一异常在CU发病中的作用值得进一步研究.     

红斑狼疮皮损中CD4~+、CD8~+ T细胞表达及其与Bcl-2关系的研究

目的:确定Bcl-2及CD4 、CD8 T细胞在红斑狼疮皮损区的表达并探讨其与红斑狼疮发病的关系.方法:采用免疫组化法对30例红斑狼疮皮损区T细胞亚群CD4 、CD8 T细胞及淋巴细胞Bcl-2进行检测,并与17例正常皮肤作对照.结果:红斑狼疮患者皮损中Bcl-2淋巴细胞和CD4 T细胞的表达明显高于正常对照组,而CD8 T细胞表达明显低于正常对照组;Bcl-2的表达与CD4 T细胞表达呈正相关,与CD8 T细胞表达呈负相关.结论:红斑狼疮皮损区淋巴细胞Bcl-2的表达增强可能会导致CD4 和CD8 T细胞凋亡异常,从而导致免疫紊乱而发病.     

系统性红斑狼疮患者外周血CD4+、CD8+T细胞p16基因mRNA表达

目的:探讨p16基因mRNA在系统性红斑狼疮(SLE)患者CD4+、CD8+T细胞中的表达.方法:收集40例确诊的SLE患者(患者组)和30名正常人(对照组)外周血,应用免疫磁珠法分选CD4+、CD8+细胞并计数,提取RNA,应用实时定量RT-PCR方法检测外周血CD4+、CD8+T细胞中p16基因mRNA表达水平.结果:①p16基因mRNA在CD4+T细胞中的表达:分别与对照组(2.245±0.586)和SLE非活动期组(1.361±0.154)相比较,SLE活动期组(93.264±42.898)明显增加,差异均具有统计学意义;而非活动期组与对照组之间差异无统计学意义.②p16基因mRNA在CD8+T细胞中的表达:分别与对照组(4.323±0.735)和非活动期组(3.722±1.701)比较,SLE活动期组(92.926±38.102)明显增加,差异均具有统计学意义;而非活动期组和对照组之间差异无统计学意义.结论:SLE患者p16基因mRNA水平在CD4+、CD8+T细胞中增高,提示SLE患者存在p16基因表达异常.     

结缔组织疾病

20053223异基因小鼠胚胎胸腺移植治疗系统性红斑狼疮模型鼠的实验观察/徐高四(江西医学院上饶分院免疫学教研室),刘巧云,曹会生…∥中国皮肤性病学杂志.-2005,19(6).-336~33721只符合要求的BALB/C×C57BL/6F1小鼠经尾静脉注射亲代淋巴细胞混悬液后随机分成3(A~C)组,于SLE模型建立成功后接受相应治疗方案,第25天处死模型小鼠,采用流式细胞术检测各组小鼠外周血中CD4+/CD8+细胞比值。C组外周血中CD4+/CD8+T细胞的比值显著高于A组(P<0.05),但A组与B组相比,差异无显著性(P>0.05)。B组胸腺指数与A组相比,差异无显著性(P>0.05),但显…     

他克莫司软膏对银屑病患者皮损T细胞的影响

目的观察他克莫司软膏对银屑病皮损处T细胞的影响。方法采用免疫组化法检测10例寻常性银屑病(斑块型)患者应用0.1%他克莫司软膏治疗前、后的皮损组织及10例正常健康人的皮肤组织中CD3,CD4及CD8T细胞的表达。结果 0.1%他克莫司软膏治疗后,银屑病皮损的表皮层CD3,CD4及CD8T细胞降低不明显,真皮层CD3,CD4及CD8T细胞的表达明显减少。结论他克莫司软膏对银屑病皮损处CD3+、CD4+和CD8+T细胞有显著的抑制作用。     

银屑病皮损CD8αα+ T细胞表型鉴定

目的 探究银屑病皮损局部浸润的CD8+ T细胞表型及其在银屑病发病中的作用。方法 收集2017年1 - 12月第四军医大学西京皮肤医院明确诊断的8例进行期斑块状银屑病患者皮损,男女各4例,年龄24 ~ 50岁。8例健康对照皮肤来源于整形外科手术剩余皮肤,男女各4例,年龄23 ~ 46岁。采用免疫荧光技术检测皮损CD8+ T细胞的分布及亚群比例,鉴定其免疫学表型及炎症因子白细胞介素（IL）17A的表达。结果 8例银屑病皮损真、表皮均可见CD8+ T细胞浸润,其中CD8αα+ T细胞表型占88.48% ± 7.39%,8例健康人皮肤局部仅有个别CD8+ T细胞浸润,其中CD8αα+ T细胞表型占14.43% ± 13.14%,两组比较,t = 11.5,P < 0.01。银屑病皮损表皮CD8αα+ T细胞表达组织局部定植标志CD103,真皮CD8αα+ T细胞不表达CD103。银屑病皮损CD8αα+ T细胞表达CD45RA-CCR7-效应记忆性T细胞表型,不表达CD8+ 调节性T细胞标志Foxp3、CD25和CD122。银屑病皮损CD8αα+ T细胞中分泌IL?17A的细胞比例为24.85% ± 4.25%,对照组CD8αα+ T细胞不分泌IL?17A,两组差异有统计学意义（t = 5.853,P < 0.01）。结论 银屑病皮损浸润的CD8αα+ T细胞是效应记忆性T细胞,可能通过分泌IL?17A参与银屑病的发生发展。     

Defective functions of circulating CD4+CD25+ and CD4+CD25- T cells in patients with chronic ordinary urticaria

BACKGROUND: Patients with chronic ordinary urticaria (CU) are divided into two groups: 30-50% have chronic autoimmune urticaria, and the remainder have chronic idiopathic urticaria. CD4(+)CD25(+) regulatory T (Treg) cells play critical roles in maintaining peripheral tolerance and preventing autoimmunity, but the characteristics of Treg cells have not yet been defined in CU. OBJECTIVE: To identify whether CD4(+) T cells play an important immunoregulatory role in the etiology of CU, we determined the frequencies and functions of circulating CD4(+)CD25(+) and CD4(+)CD25(-) T cells in CU patients and healthy control subjects, with special focus on the characteristics of CD4(+)CD25(+) T cells. METHODS: Peripheral blood mononuclear cells (PBMCs) were obtained from CU and healthy controls in this study. The frequency of CD4(+)CD25(+) T cells in PBMCs was detected by flow cytometry. The expression levels of forkhead box P3 (FOXP3) and transforming growth factor-beta (TGF-beta) in CD4(+)CD25(+) T cells were detected by real-time PCR. Furthermore, the suppressive function of CD4(+)CD25(+) T cells was analyzed. Additionally, the Th1/Th2 cytokine secretory profile in mitogen-stimulated CD4(+)CD25(-) T cells was measured by ELISA. RESULTS: An increased frequency of CD4(+)CD25(+) T cells was observed in CU patients (n=19) compared to control subjects (n=7). No significant difference was detected in the expression levels of FOXP3 or TGF-beta between CU patients (n=14) and control subjects (n=7). Strikingly, the suppressive capacity of CD4(+)CD25(+) Treg cells from 2 of 5 CU patients was partially defective. We also found that cytokine production from CD4(+)CD25(-) T cells was significantly reduced in CU patients (n=9) compared to healthy donors (n=11). CONCLUSIONS: Our data demonstrate that CD4(+)CD25(+) and CD4(+)CD25(-) T cells in PBMCs exhibit defective functions in CU patients.     

不同等级宫颈病变患者炎性因子、T细胞亚群、阴道菌群情况研究

目的:探究CIN或宫颈癌患者阴道菌群、宫颈局部T细胞亚群以及血清炎性因子的组成,为宫颈癌的防治提供新的思路。方法:选取2013年8月至2015年7月我院收治的HPV阳性且病理活检确诊为CIN或宫颈癌的患者200例作为观察组,同时选取HPV阴性且宫颈活检正常者120例作为对照组。两组患者均于初诊时留取阴道分泌物、宫颈分泌物及脱落细胞、宫颈组织标本,采用液基薄层细胞学检查法(TCT)检测宫颈病变程度,采用悬滴湿片法检测滴虫,革兰氏染色检测霉菌、淋球菌和乳酸杆菌等;采用免疫组化法检测宫颈CD4~+和CD8~+T淋巴细胞的表达;采用酶联免疫吸附法(ELISA)检测血清炎性因子IL-2、IL-4、IL-10、IFN-γ和TNF-α。结果:两组患者在解脲支原体、衣原体的感染率以及乳酸杆菌的阴性感染率之间差异具有统计学意义(P0.05),且随着病变程度的加重,其感染率也存在明显差异,而其它病原体感染在两组间无统计学差异(P0.05);在对照组、CINⅠ~CINⅢ以及宫颈癌患者的宫颈分泌物中CD4~+T细胞表达率呈下降趋势,而CD8~+T细胞表达率无明显差异(P0.05),但CD4~+/CD8~+的比值呈下降趋势;在对照组、CINⅠ~CINⅢ及宫颈癌患者的血清IFN-γ和IL-2水平呈下降趋势,IL-4的含量呈上升趋势,而TNF-α和IL-10的含量无明显差别(P0.05)。结论:解脲支原体、衣原体感染的增加、乳酸杆菌的减少、CD4~+T细胞表达减少可能促进宫颈病变的发生发展。     

盐酸奥洛他定联合卡介菌多糖核酸对慢性自发性荨麻疹的疗效观察

目的:探讨盐酸奥洛他定联合卡介菌多糖核酸对慢性自发性荨麻疹的疗效观察.方法:将90例慢性自发性荨麻疹患者随机分成观察组47例和对照组43例,观察组采用口服盐酸奥洛他定片联合肌内注射卡介菌多糖核酸注射液治疗,疗程为12周.对照组单纯口服盐酸奥洛他定片,用法、用量及疗程同观察组.采用荨麻疹活动度评分对两组患者治疗效果进行评...     

T、B、NK细胞亚型与慢性荨麻疹发病机制的关系

目的 探讨T、B、NK细胞亚型与慢性荨麻疹发病机制的关系。方法 用流式细胞仪检测51例慢性荨麻疹患者和30例健康献血者外周血CD3+、CD4+、CD8+ T细胞、B细胞、NK细胞的构成比，并计算CD4+/CD8+比值，分析其与病情、病程和抗组胺治疗之间的关系。结果 慢性荨麻疹患者CD8+ T细胞构成比27.20% ± 8.22%低于正常人对照组29.9% ± 3.74%（P < 0.05），CD4+/CD8+比值（1.48 ± 0.62）、NK细胞构成比21.20% ± 10.84%高于正常人对照组（分别为1.24 ± 0.27，17.5% ± 3.56%，P < 0.05）；抗组胺治疗无效组CD3+ T细胞61.81% ± 11.70%、CD8+ T细胞24.00% ± 7.79%、B细胞10.78% ± 2.07%构成比低于抗组胺治疗显效组（分别为75.74% ± 2.36%，34.22% ± 9.30%，15.25% ± 4.10%；P < 0.05，P < 0.01， P < 0.05），CD4+/CD8+比值（1.67 ± 0.76）、NK细胞构成比28.61% ± 12.62%均高于抗组胺治疗显效组（分别为1.17 ± 0.41，12.78% ± 6.02%，P < 0.01）。慢性荨麻疹患者的CD3+、CD8+ T细胞构成比与症状评分呈负相关性（r = -0.31，-0.28，P < 0.05），B细胞构成比与症状评分、病程呈正相关性（r = 0.53，0.55，P < 0.01）。结论 慢性荨麻疹患者存在T、B、NK细胞亚型构成紊乱，在慢性荨麻疹及其耐抗组胺的发病机制中，可能有体液免疫参与。     

Cytokine production of CD4+ and CD8+ peripheral T lymphocytes in patients with chronic idiopathic urticaria

The aim of this study was to investigate the characteristic cytokine pattern of patients with chronic idiopathic urticaria. Using flow cytometry, we examined the frequency of IL4, IL-10, IL-13 and IFN-gamma producing CD4+ and CD8+ T cells in the peripheral blood mononuclear cells at a single cell level. In patients with chronic idiopathic urticaria, the frequency of IL-10 producing CD4+ and CD8 + T cells was significantly higher than that of control subjects, while the frequency of IFN-y producing helper and cytotoxic T cells was significantly lower. The proportion of IL-4 producing CD4 + T cells from patients with urticaria was significantly lower. The ratio of IL-4 producing CD8 + T cells and the proportion of IL-13 producing CD4 + and CD8 + T lymphocytes did not show any significant difference between patients and controls. In our study, we could observe neither a dominant Th1 nor a dominant Th2 type cytokine pattern. We found a significant elevation in the intracellular IL-10 level which may be the cause of the down-regulated Th1 and Tc1 and partly Th2 lymphocyte functions.     

β2-integrins in different forms of urticaria

As urticarial lesions involve tissue invasion by inflammatory cells, and as β₂-integrins play a central part in adhesion of leucocytes to endothelia, allowing their migration into the tissues, we have explored the distribution and sequential expression of these molecules in tissue sections from different forms of urticaria. Prick test weals (of 10 min duration) to common inhalant allergens showed only a minor increase of CD18, whereas in a case of cold urticaria CD11b and CD18 molecules were increasingly upregulated within the first 30 min after elicitation of the lesions. Skin test sites in delayed pressure urticaria, and urticarial esions (> 6 h duration) of acute and chronic recurrent urticaria also showed marked upregulation of CD11b and CD18, and to a lesser extent of CD11a, but this did not strongly correlate with the intensity of the mixed cellular infiltrate. Non-lesional skin showed expression of β₂-integrins in chronic urticaria, delayed pressure urticaria, and less so in acute urticaria, suggesting generalized leucocyte activation. This analysis of integrins thus suggests an early and extensive involvement of these molecules in the pathological events associated with the evolution of urticarial lesions.     

Immunohistological study of the development of the cellular infiltrate in the pelage follicles of the DEBR model for alopecia areata

The Dundee experimental bald rat (DEBR) undergoes hair loss associated with perifollicular infiltrates of mononuclear cells (MNC), a pathological characteristic of human alopecia areata (AA). To investigate further the pathogenesis of the disease in this animal model, we have studied the development, composition and extent of the perifollicular MNC infiltration in young (6-week-old), prelesional (3-month-old), active lesional, and established lesional DEBR rats, using 6-week- and 6-month-old Wistar rats as normal controls. The proportions of hair follicles showing infiltration by MNC and their main subsets were determined using immunohistochemical staining of serial cryostat sections of flank skin biopsies. There was a good correlation between the degree of leucocyte (OX-1⁺) infiltration of anagen hair follicles and the development of hair loss. In 6-week-old DEBR skin, there were few perifollicular cells expressing MHC class II, with positively stained dendritic cells in the dermis above the sebaceous gland. There was a sparse perifollicular distribution of CD4⁺ cells (W3/25) and macrophages (ED-1⁺). No CD8⁺ cells (OX-8⁺) were seen associated with DEBR hair follicles, and only small numbers were present in Wistar rats. In prelesional DEBR rats there was an increased perifollicular presence of MHC class II⁺ cells, macrophages, and particularly of CD8⁺ cells, with little change in CD4⁺ cells. Active and established lesional rats, i.e. animals with overt loss of hair, showed a significant increase in the degree of MNC infiltration and the proportion of infiltrated follicles, the majority of which were in dystrophic anagen. In the perifollicular infiltrate the CD4⁺:CD8⁺ ratio was approximately 2:1. An intrafollicular infiltrate was prominent, and was composed of CD8⁺ cells and macrophages, with bulbar and suprabulbar keratinocytes expressing MHC class II antigens. CD4⁺ cells were not detected in follicular epithelium. ICAM-1 expression correlated with MNC infiltration. These results show marked similarities to lesional human AA. They also focus on a possible active role for CD8⁺ cells in the pathogenesis of hair loss in the DEBR rat.     

Immunologic Principles of Allergic Disease

Allergy either results from a pathological excessive immune reaction, or from the defective induction of tolerance to otherwise harmless antigens. Allergic reactions are mounted by mechanisms of innate and adaptive immunity. The development of an allergic response can be divided in sensitization and elicitation phases. Immediate type allergic reactions (e.g. anaphylaxis, urticaria, rhinoconjunctivitis allergica, allergic asthma) are mediated by IgE antibodies which are produced by B cells stimulated by allergen‐specific Th2 cells. Crosslinking of allergen‐specific IgE on membrane surfaces of mast cells and basophilic granulocytes leads to release of soluble mediators which may cause systemic symptoms within minutes to hours. The following infiltration of eosinophilic granulocytes and Th2 cells directs chronic inflammation. Humoral cytotoxic immune reactions (e.g. drug induced cytopenia) are mediated by IgG and IgM antibodies which are directed against membrane associated antigens. IgG and IgM antibodies directed against soluble antigens elicit immune complex mediated cytotoxicity (e.g.drug induced vasculitis).Delayed type immune reactions (e.g.contact dermatitis) are based on the activation of antigen specific CD4⁺ and CD8⁺ T cells and need 24 h to 48 h to develop. Upon recurrent contact with identical antigens, recruitment of CD4⁺ and CD8⁺ T cells cause inflammation and cytotoxic induced apoptosis in target cells as well as cytokine mediated leukocyte infiltration. Subsequent immigration of CD4⁺ Th2 cells provides anti‐inflammatory mechanisms leading to resolution of the inflammatory response and tissue repair.     

Immunophenotyping of inflammatory cells in lesional skin of the extrinsic and intrinsic types of atopic dermatitis

BACKGROUND: There is a subgroup of atopic dermatitis (AD) patients with normal total and specific IgE levels and negative skin tests towards common allergens. This form of the disease has been referred to as the 'intrinsic' form of AD. Although previous studies have demonstrated differences in the cytokine profile between the extrinsic and intrinsic subtypes, the pathogenesis of both subtypes of AD remains unclear. OBJECTIVES: To compare the inflammatory micromilieu in both forms of AD. METHODS: Immunophenotyping of the inflammatory cells was performed in lesional and nonlesional skin from 18 patients with extrinsic and 17 with intrinsic AD. RESULTS: Immunohistochemical analysis revealed a high proportion of CD4+ T cells in the dermis, with a similar CD4/CD8 ratio in the two groups. The expression levels of other T-cell markers and epidermal Langerhans cells were increased in both forms of AD. Although the T-cell repertoires in the two subtypes were similar, dermal infiltration of eosinophils and eosinophil granular proteins was more prominent in the extrinsic type than in the intrinsic type. Eotaxin immunoreactivity was also significantly higher in the extrinsic subtype. CONCLUSIONS: The data suggest that although the overall inflammatory microenvironment in the two subtypes appears to be similar, differences in T-cell cytokine production might contribute to the differential tissue eosinophilia in these subtypes.     

Detection of CD4+ CD25+ FOXP3+ regulatory T cells in peripheral blood of patients with chronic autoimmune urticaria

Background/Objectives: Compelling evidence indicates a significant role for a population of CD4⁺ T regulatory cells in suppressing immune responses and in maintaining immunological homeostasis. This study aims to investigate the potential role of CD4⁺CD25^HIGHFOXP3⁺ T regulatory cells in patients with chronic autoimmune urticaria and to define the characteristics of CD4⁺CD25^HIGHFOXP3⁺ cells in chronic urticaria. Methods: We used flow cytometry to assess the expression of CD4⁺CD25^HIGHFOXP3⁺ cells in the peripheral blood mononuclear cells of patients with chronic autoimmune urticaria. Results: In this study, we found that patients with chronic autoimmune urticaria have a significantly reduced frequency of CD4⁺CD25^HIGHFOXP3⁺ cells (1.39 ± 0.27% vs 2.09 ± 0.34%; P = 0.001) in their peripheral blood, accompanied by a decreased intensity of FOXP3 expression (50.13 ± 9.79 vs 68.19 ± 6.40; P < 0.001). Notably, although patients with chronic idiopathic urticaria had a reduced frequency of CD4⁺CD25^HIGHFOXP3⁺ cells (1.85 ± 0.46% vs 3.64 ± 0.48%; P < 0.001), their FOXP3 expression levels did not differ from those in healthy controls. Conclusions: Patients with chronic autoimmune urticaria displayed a reduced percentage of CD4⁺CD25⁺FOXP3⁺ regulatory T cells. The results imply CD4⁺CD25⁺FOXP3⁺ regulatory T cells may contribute to the autoimmune pathological process of chronic autoimmune urticaria.