银屑病患者骨髓CD34+细胞体外定向分化的T细胞活性研究

目的 研究有家族发病倾向的银屑病患者骨髓CD34⁺细胞体外定向发育的T细胞活性.方法 免疫磁珠法分离家族史阳性银屑病患者及正常对照骨髓CD34⁺细胞,在骨髓基质细胞条件培养液构建的微环境下,在胸腺基质细胞的支持下,使其在体外向T细胞定向分化,免疫磁珠法收集CD3⁺T细胞,流式细胞仪检测CD4⁺CD8^-细胞及CD4^-CD8⁺细胞比例.分别采用MTT法及ELISA法检测自然增殖组及链球菌超抗原刺激后T细胞增殖活性及分泌细胞因子水平.结果 ①经骨髓CD34⁺细胞定向分化并扩增的CD3⁺T细胞中可检测到CD4⁺CD8^-、CD4^-CD8⁺T细胞,且银屑病患者组与正常对照组CD4⁺CD8^-及CD4^-CD8⁺T细胞比例无显著差异.②银屑病患者骨髓CD34⁺细胞定向分化的T细胞自然增殖组及链球菌超抗原刺激组增殖活性均显著高于正常人对照组.③银屑病患者T细胞自然增殖组培养上清白介素4、白介素8及干扰素γ与正常对照组差异无统计学意义,链球菌超抗原刺激后白介素4表达水平无显著改变,而白介素8及干扰素γ水平却显著高于正常人.结论 有家族发病倾向的银屑病患者外周血T细胞活性异常可能与骨髓造血细胞相关.     

女性生殖道尖锐湿疣患者外周血淋巴细胞B7-CD28/CTLA-4的表达及意义

目的 探讨B7-CD28/CTLA-4(CD152)T淋巴细胞活化协同刺激分子在女性生殖道尖锐湿疣发病、发展及转归中的作用.方法 用流式细胞仪检测30例女性生殖道尖锐湿疣患者和15例正常人外周血淋巴细胞中CD80/CD86及CD4⁺/CD8⁺T淋巴细胞中CD28/CD152(CTLA-4)的表达.结果 CD80/CD86及CD4⁺、CD8⁺/CD28阳性表达水平初发组(17例)、复发组(13例)与正常人对照组(15例)比较,差异无统计学意义;恢复组(15例)CD4⁺、CD8⁺/CD28及CD80阳性表达水平分别较复发组明显增高(P<0.05).CD4⁺、CD8⁺/CD152在尖锐湿疣复发组和初发组阳性表达水平均较正常人对照组明显增高(P<0.05),且复发组较初发组进一步增高,两组比较差异有统计学意义(P<0.05);恢复组CD4⁺、CD8⁺/CD152阳性表达水平较初发组及复发组明显降低(P<0.05),与正常人对照组比较差异无统计学意义.结论 女性生殖道尖锐湿疣患者外周血淋巴细胞和CD4⁺、CD8⁺T淋巴细胞中B7-CD28/CTLA-4(CD152)表达异常,并与其病程发展关系密切.     

自体疣植入治疗扁平疣及其相关机制研究

目的 应用自体疣植入治疗扁平疣,研究患者T细胞亚群和白介素2(IL-2)水平的变化以及疣体脱落的病理和免疫学特征。方法 采用单克隆抗体碱性磷酸酶-抗碱性磷酸酶(APAAP)法和放射免疫法检测患者外周血T细胞亚群及IL-2水平;对反应期疣体组织进行常规HE染色和免疫组织化学分析。结果 治疗前外周血CD4⁺细胞数、CD4⁺/CD8⁺比值及IL-2水平均明显低于正常人对照组(P<0.01);治疗后均显著升高(P<0.01),与正常人对照组差异无显著性(P>0.05)。反应期疣体组织中见淋巴细胞浸润,伴棘细胞水肿、溶解。免疫组化显示,反应区浸润的淋巴细胞主要呈CD45RO⁺、CD6⁺、CD4⁺、CD8⁺、CD20^-和Mac387^-;在表皮基底层及反应区可见S-100蛋白阳性的朗格汉斯细胞。结论 自体疣植入治疗扁平疣能增强细胞免疫功能,通过T细胞介导免疫反应使CD8⁺亚群发挥细胞毒性作用,导致疣体脱落。     

SLE患者T淋巴细胞穿孔素基因启动子区域甲基化状态的探索

目的 探讨系统性红斑狼疮(SLE)T淋巴细胞穿孔素基因启动子区域DNA甲基化状态及其在发病机制中的作用.方法 分离9例活动期SLE患者和7例正常人对照外周血CD4⁺与CD8⁺T细胞,并分别提取DNA.采用亚硫酸氢钠-测序法对CD4⁺与CD8⁺T细胞穿孔素基因启动子区域DNA甲基化水平进行检测.结果 在穿孔素基因启动子区域,正常对照组CD4⁺T细胞平均甲基化水平显著高于CD8⁺T细胞(P<0.05).活动期SLE患者CD4⁺T细胞平均甲基化水平显著低于正常对照组(P<0.05),而CD8⁺T细胞与正常对照组的差异则无统计学意义(P>0.05).结论 活动期SLE患者的CD4⁺T淋巴细胞的穿孔素基因启动子区域处于低甲基化状态.     

皮肤结节性血管炎患者Th1/Th2型细胞因子表达的研究

目的 探讨CD3⁺、CD4⁺和CD8⁺T细胞和IL-2、IL-4、IL-6及sIL-2R与结节性血管炎患者发病、疾病活跃程度的关系。方法 采用流式细胞仪及ELISA法检测外周血CD3+、CD4⁺、CD8⁺T细胞亚群,血清IL-2、IL-6及sIL-2R水平,用链霉亲和素-过氧化物酶(SP)法检测皮损组织局部CD3⁺、CD4⁺、CD8⁺T细胞亚群浸润及IL-2、IL-4表达水平。结果 活动期结节性血管炎患者血清IL-2、IL-6及sIL-2R水平高于非活动期和正常人对照组;而外周血CD3⁺、CD4⁺、CD8⁺T细胞亚群与消退期及正常人比较差异无显著性。病变组织中CD3⁺、CD4⁺T细胞和IL-2染色阳性细胞高于正常人对照组;IL-4染色阳性细胞与正常人对照组差异无显著性。结论 IL-2为代表的Th1细胞因子可能参与结节性血管炎的发病机制,血清及组织浸润IL-2水平与疾病活跃相关。     

寻常型银屑病皮肤中皮肤归巢T细胞免疫组化研究

目的 探讨皮肤归巢T细胞在寻常型银屑病(PV)发病中的作用。方法 采用间接免疫荧光双标法研究正常人皮肤和PV患者皮肤中浸润的皮肤归巢T细胞分类及其变化。结果 ①正常人皮肤及PV皮损中浸润的T细胞绝大多数表达皮肤淋巴细胞相关抗原(CLA),CLA⁺细胞高度表达CD45RO,只有个别为CD45RO阴性。②进行期皮损CD4⁺CLA⁺及CD8⁺CLA⁺T细胞数高于静止期皮损(P<0.05),静止期皮损CD4⁺CLA⁺细胞数高于消退期皮损(P<0.05),消退期皮损CD8+CLA+细胞数高于PV外观正常皮肤(P<0.05),进行期皮损周边外观正常皮肤CD4⁺CLA⁺及CD8⁺CLA⁺细胞数高于静止期皮损周边外观正常皮肤(P<0.05).③部分病例皮损的表皮中见大量CLA⁺树突状细胞,正常人皮肤未见此细胞。结论 正常人皮肤及PV皮损中T细胞绝大多数为皮肤归巢T细胞;进行期及静止期PV皮损中浸润的细胞主要为CD3⁺、CD4⁺、CD45RO⁺、CLA⁺T细胞,CD3⁺、CD4⁺、CD45RO⁺、CLA⁺T细胞可能在PV发病中起重要作用。     

尖锐湿疣患者外周血CD8+T细胞细胞因子的表达

目的 检测尖锐湿疣患者外周血CD8⁺T细胞白介素-2、白介素-12、干扰素-γ、白介素-4的表达水平,探讨其在尖锐湿疣发病中的作用.方法 应用流式细胞仪检测60例尖锐湿疣患者和20例正常人对照者外周血CD8⁺T细胞白介素-2、白介素-12、干扰素-γ、白介素-4的表达水平.结果 尖锐湿疣患者外周血CD8⁺T细胞白介素-2、白介素-12、干扰素-γ阳性细胞百分比均显著下降(P<0.01);白介素-4+CD8⁺T细胞百分比与正常人对照组比较,差异无统计学意义(P>0.05);干扰素-γ+/白介素-4+T细胞比值显著低于正常人对照组(P<0.01).结论 尖锐湿疣患者Tc1细胞水平低下,Tc1/Tc2显著低于正常人对照.     

二期梅毒患者外周血淋巴细胞凋亡及其Fas、Bcl-2表达的研究

目的 检测二期梅毒患者外周血淋巴细胞(PBLC)凋亡及其Fas、Bcl-2的表达,探讨二期梅毒患者免疫功能异常与淋巴细胞凋亡的关系。方法 采用流式细胞仪检测33例二期梅毒患者和30例正常人PBLC细胞凋亡及其Fas、Bcl-2的表达。结果 梅毒患者PBLC及CD4⁺细胞Fas表达明显高于对照组(P<0.01),而Bcl-2表达明显低于对照组(P<0.01)。CD8⁺、CD19⁺细胞Fas、Bcl-2表达两组比较差异无统计学意义(P>0.05)。梅毒患者PBLC及CD4⁺细胞凋亡率显著高于对照组(P<0.01),CD8⁺及CD19⁺细胞凋亡率两组比较差异无统计学意义(P>0.05)。梅毒患者PBLC及CD4⁺细胞凋亡率分别与其Fas表达呈显著正相关(r=0.68,P<0.01;r=0.71,P<0.01),但与Bcl-2表达呈显著负相关(r=-0.82,P<0.01;r=-0.74,P<0.01)。结论 二期梅毒患者细胞免疫功能异常可能与淋巴细胞凋亡过度有关,而淋巴细胞凋亡过度与Fas、Bcl-2表达异常有关。     

复发性生殖器疱疹患者外周血单一核细胞CD40和CD40L的表达

目的 探讨复发性生殖器疱疹患者外周血单一核细胞CD40、CD40L的表达。方法 利用流式细胞仪对30例复发性生殖器疱疹患者和20例正常人对照者外周血单一核细胞(PBMC)CD40、CD40L的表达及T淋巴细胞亚群进行检测。结果 病例组PBMC中CD40阳性细胞百分数较对照组显著降低(P=0.0061);CD40L阳性细胞百分数较对照组明显降低(P=0.041);CD3⁺T细胞和CD4⁺T细胞百分数亦显著低于对照组(其P值分别为0.025和0.032)。结论 CD40-CD40L共刺激作用低下是生殖器疱疹复发的重要原因之一。     

皮肤淀粉样变性皮损中T/B细胞的检测

目的 探讨原发性皮肤淀粉样变性皮损中T/B细胞变化的差异及其意义.方法 60例患者局部病变皮损标本、29例正常人皮肤标本,分别进行CD3、CD4、CD8、CD20免疫组化染色.结果 与正常人对照组比较,皮肤淀粉样变性皮损中,淋巴细胞总数、CD3⁺T细胞、CD8⁺T细胞的均数增高(P<0.05),CD4⁺T细胞均数无明显增高(P>0.05),CD4⁺/CD8⁺T细胞比值下降(P<0.05),CD20⁺B细胞均数增高(P<0.05).T淋巴细胞、B淋巴细胞在原发性皮肤淀粉样变性苔藓样、斑疹型或双相型三种分型病变间相互比较,差异无统计学意义(P>0.05).结论 原发性皮肤淀粉样变性局部皮损存在有T/B淋巴细胞的异常表达,但三种病变类型间病变机制的免疫学异常无区别.     

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。     

Reduced CD26bright expression of peripheral blood CD8+ T-cell subsets in psoriatic patients

Abstract: Background: T cells have been shown to be highly relevant in psoriasis. CD26 is a novel T‐cell activation marker involved in various T‐cell functions, e.g. (i) co‐stimulation, (ii) migration and (iii) T‐cell memory response. In particular, CD26bright peripheral blood T cells have been shown to be altered in several autoimmune diseases. Objective: To characterize CD26‐expression of T‐cell subsets in psoriatic patients compared to healthy subjects. Methods: Peripheral blood was obtained from 15 untreated patients with severe psoriasis and from nine healthy subjects. The presence of specific CD26‐related T‐cell subsets was assessed by flow cytometry. Results: The CD26bright expression of CD8+ lymphocytes revealed a statistically significant (P<0.05) decrease in psoriatic patients. The majority of CD4+CD26bright cells are CD45RO+, whereas the minority of CD8+CD26bright cells are CD45RO+ in both groups. Conclusions: The present study demonstrates that the CD8CD26bright T‐cell population is markedly decreased in peripheral blood of psoriatic patients. Moreover, CD26 expression did not show a restriction to memory T cells. As CD26 is of relevance for T‐cell functions, future investigations should focus on elucidating these functions in psoriasis. It is attractive to speculate that the reduction in the CD8CD26bright subpopulation may represent a biomarker for recompartimentalization of activated T cells and a reduced CD8CD26bright count may correlate with increased responsiveness to T‐cell targeted treatments.     

Functional characterization of CD4+CD25+ regulatory T cells differentiated in vitro from bone marrow-derived haematopoietic cells of psoriasis patients with a family history of the disorder

BACKGROUND: In psoriasis CD4+CD25+ regulatory T cells are functionally deficient. The imbalance between regulatory and effector T-cell functions is important for inducing psoriasis. It is reasonable to speculate that the dysfunctional activity of CD4+CD25+ regulatory cells may originate partly from the abnormal haematopoietic cells determined mainly by genetic background. OBJECTIVES: To test the hypothesis that haematopoietic stem cells are responsible for dysfunctional CD4+CD25+ regulatory cells in psoriasis. METHODS: Bone marrow-derived CD34+ haematopoietic cells from patients with psoriasis (with a family history of psoriasis) and from normal controls were differentiated into T cells in vitro. CD4+CD25+ T cells were isolated by an immunomagnetic bead method, and proliferation activity and capacity for cytokine secretion were determined. Furthermore, the ability of CD4+CD25+ T cells to suppress the proliferative responses of allogeneous peripheral blood CD4+CD25- effector T cells was assessed in vitro. RESULTS: The differentiated CD4+CD25+ T cells of psoriatic origin showed similar characteristics to those of normal volunteers, including proliferation activity and secretion profile of the cytokines interleukin (IL)-2, IL-4, IL-8, IL-10 and interferon (IFN)-gamma. However, proliferation and secretion levels of the cytokines IL-2 and IL-10 for CD4+CD25+ cells of psoriatic CD34+ cell origin were significantly lower than those of normal controls in response to streptococcal superantigen (Strep-A). In particular, CD4+CD25+ T cells differentiated from psoriatic CD34+ cells were functionally insufficient to restrain effector T-cell proliferation. CONCLUSIONS: CD4+CD25+ T cells differentiated in vitro from haematopoietic cells of patients with psoriasis are impaired in regulatory function. The dysfunction of psoriatic CD4+CD25+ T cells may be due to inherent genetic programming passed down from bone marrow-derived haematopoietic cells.     

Increased expression of the natural killer cell inhibitory receptor CD94/NKG2A and CD158b on circulating and lesional T cells in patients with chronic plaque psoriasis

BACKGROUND: Psoriasis is a common inflammatory cutaneous disorder characterized by activated T-cell infiltration. T lymphocytes bearing natural killer cell receptors (NKRs) have been suggested to play an important role in the pathogenesis of psoriasis. However, the expression pattern of activating and inhibitory NKRs on T lymphocytes from psoriatic patients and its significance in psoriasis needs further study. OBJECTIVES: To investigate the pathogenesis of NKR-expressing T cells in psoriasis. MATERIALS AND METHODS: Thirty patients with chronic plaque psoriasis and 20 healthy controls were enrolled in this study. The immunophenotypic profiles of NKRs, including CD56, CD16 (activating NKRs), CD158a, CD158b, CD94 and NKG2A (inhibitory NKRs), were analysed in peripheral blood T lymphocytes, as well as psoriatic lesional infiltrating T cells, by triple-fluorescence flow cytometry. RESULTS: A significant increase of inhibitory CD8+ CD158b+, CD4 CD8 CD158b+ and CD8+ CD94/NKG2A+ T cells was found in the peripheral blood of patients with psoriasis when compared with controls. Tissue-infiltrating T lymphocytes expressing inhibitory receptors CD158b, CD94 and NKG2A were found in psoriatic lesions. There was a significant positive correlation between the increased percentage of circulating CD8+ CD94/NKG2A+ T cells and the Psoriasis Area and Severity Index. CONCLUSIONS: In the present study, we demonstrated increased proportions of particular subsets of inhibitory CD158b+ and/or CD94/NKG2A+ T cells in patients with psoriasis. The elevation of these inhibitory NKR-expressing T cells was correlated with disease severity, which may signify the possibility of chronic antigen-driven stimulation and dysregulated cytokine production in the pathogenesis of psoriasis.     

Dramatic improvement of psoriatic erythroderma after acute hepatitis: analysis of cytokine synthesis capability in peripheral blood T cells

We report a patient with psoriasis and hepatitis C virus infection who initially presented with psoriatic erythroderma and eventually showed complete clearance of psoriatic lesions following acute hepatitis induced by etretinate treatment. Cytokine synthesis capabilities in peripheral blood T cells obtained at different stages were evaluated in this patient. A dramatic increase in the frequency of interferon-gamma-producing CD8+ T cells in peripheral blood was observed during the erythrodermic stage. In contrast, the frequencies of interleukin (IL)-4- and IL-13-producing CD4+ T and CD8+ T cells were remarkably high at the resolution stage. These results clearly indicate that a shift towards type 2 cytokine predominance contributes to the resolution of severe psoriasis.     

流式细胞术双色免疫荧光标记观察寻常性银屑病患者外周血淋巴细胞亚群

目的了解寻常性银屑病患者外周血淋巴细胞亚群的变化。方法应用流式细胞仪双色免疫荧光标记,检测98例寻常性银屑病患者外周血淋巴细胞亚群并与102名正常人进行比较。结果银屑病患者外周血CD4+细胞百分数显著高于正常人对照组(P<0.05);NK细胞百分数显著低于正常人对照组(P<0.01),寻常性进行期银屑病患者T细胞和CD4+细胞显著高于静止期银屑病患者(P<0.05),进行期银屑病患者T细胞、B细胞、CD4+细胞百分数均显著高于正常人对照组(P<0.001),NK细胞显著低于正常人对照组(P<0.001)。静止期银屑病患者与正常人对照组相比淋巴细胞亚群各项指标无明显差异。结论寻常性银屑病患者外周血淋巴细胞亚群的变化主要表现在T、B淋巴细胞特别是CD4+细胞的升高和NK细胞的降低。     

寻常型银屑病患者外周血CD4~+CD25~+及CD8~+CD25~+细胞的检测

目的研究进展期寻常型银屑病患者外周血CD4+CD25+和CD8+CD25+调节性T细胞的数量变化及其在银屑病免疫病理学发病机制中的作用。方法应用流式细胞术对进展期寻常型银屑病患者外周血CD4+CD25+和CD8+CD25+调节性T细胞进行检测。结果进展期寻常型银屑病外周血CD4+CD25+细胞及CD8+CD25+调节性T细胞数量与正常对照组相比,均显著降低(P<0.05,P<0.005),而CD4+CD25+/CD8+CD25+比值无显著性差异(P>0.05)。结论寻常型银屑病的发病与CD4+CD25+和CD8+CD25+调节性T细胞的同步降低有关,与二者的比值无关。     

Profiles of activated T lymphocytes in peripheral blood of Kuwaiti psoriasis vulgaris patients

We have previously reported unexpected immunological features of psoriasis among Kuwaitis, suggesting novel patterns of immune reactivity contributing to the disease. To better define this phenomenon, we herein describe profiles of major populations and immunologically activated subsets of peripheral blood lymphocytes in a cohort of Kuwaiti psoriasis vulgaris patients. Whole venous blood from fifteen psoriatic and twenty eight normal, healthy subjects was analyzed by 2-color flow cytometry for levels of major lymphocyte species and their immunologically activated subsets. When compared to normal subjects, psoriatic blood contained lower cell densities of CD2+, CD8+ (p=0.002 respectively) and B lymphocytes (CD19+) (p=0.003), with a trend toward a lower CD4+ density (p=0.072). Within each major lymphocyte population, activated lymphocytes were present at higher percentages in psoriatic than in healthy blood. These included CD4+ HLA-DR+ (p=0.002), CD4+CD25+ (p=0.043), CD4+CD54+ (p=0.005), CD8+CD25+ (p=0.015), CD8+ HLA-DR+ (p=0.046) and CD3+CD16+CD56+ (p=0.023) Additionally, psoriatic patients were found to have an expanded ratio of memory to naive T cells (CD45RO+CD45RA+) relative to control subjects; this was expected on the basis of increased immune activation. Our findings are consistent with a picture of psoriasis as a disease mediated by activated lymphocytes.     

银屑病患者皮损和外周血中CD8α+α+ T细胞的研究

目的 观察银屑病患者皮损和外周血中CD8α+α+ T细胞的分布和比例,探讨其在银屑病发病中的作用。 方法 采用免疫荧光技术观察5例进展期寻常性银屑病患者和5例健康人皮肤中CD8α+α+ T细胞的分布,流式细胞仪分别检测10例进展期寻常性银屑病患者和8例健康人外周血中CD8α+α+ T细胞比例及干扰素γ（IFN-γ）和肿瘤坏死因子α（TNF-α）的表达。采用Graphpad Prism统计软件对实验组和对照组各数据进行t检验。 结果 在5例银屑病患者皮损真皮浅层均可见以CD8α+α+ T细胞为主的浸润,未见明显的CD8α+β+ T细胞浸润;而5例健康人皮肤中均未见CD8α+α+ T细胞和CD8α+β+ T细胞浸润。流式细胞仪检测,8例健康人外周血中CD8α+α+ T细胞比例为9.12% ± 4.80%,10例银屑病患者组为26.47% ± 12.99%,银屑病患者组明显高于对照组,两组比较,t = 3.96,P ＜ 0.001。在银屑病患者外周血CD8α+α+ T细胞中分泌IFN-γ和TNF-α的细胞比例分别为47.36% ± 19.38%和54.14% ± 21.14%,健康对照组分别为13.44% ± 9.21%和34.03% ± 17.22%,两组差异均有统计学意义（t值分别为4.54和2.17,P值分别 ＜ 0.001和 ＜ 0.05）。 结论 银屑病患者皮损和外周血中存在CD8α+α+ T细胞的分布和比例增多,CD8α+α+ T细胞可能是参与银屑病发病的主要CD8+ T细胞亚群。     

Preferential expression of alphaEbeta7 integrin (CD103) on CD8+ T cells in the psoriatic epidermis: regulation by interleukins 4 and 12 and transforming growth factor-beta

BACKGROUND: Intraepidermal T lymphocytes are a critical element for sustaining the lesional pathology of psoriasis. Integrin alphaEbeta7 (CD103), a ligand for E-cadherin, may play a role in the localization of pathogenic T cells within the epidermis of psoriatic lesions. However, little information is available regarding alphaEbeta7 expression on intraepidermal T cells in psoriasis. OBJECTIVES: To examine alphaEbeta7 expression on intraepidermal T cells in psoriatic lesions and the regulation of alphaEbeta7 expression on T cells in response to cytokines. METHODS: T-cell expression of alphaEbeta7 was examined by immunohistochemistry and flow cytometry. In vitro regulation of alphaEbeta7 expression on CD4+ or CD8+ T cells purified from peripheral blood of healthy donors was also examined. RESULTS: Immunohistochemical staining revealed expression of alphaEbeta7 on a greater proportion of epidermal T cells than dermal T cells. Nearly 30% of intraepidermal CD4+ T cells were found to express alphaEbeta7 on flow cytometry, whereas more than 80% of intraepidermal CD8+ T cells expressed this integrin. In contrast, few T cells expressed alphaEbeta7 in the peripheral blood of psoriatic patients. The in vitro culture experiment confirmed that alphaEbeta7 was preferentially expressed on CD8+ T cells after stimulation with anti-CD3 monoclonal antibodies. Addition of transforming growth factor-beta and interleukin-4 upregulated alphaEbeta7 expression on T cells, whereas interleukin 12 downregulated this. Furthermore, alphaEbeta7 expression on established memory CD8+ T cells was not so reversible as that on CD4+ T cells. CONCLUSIONS: Preferential and stable expression of alphaEbeta7 on CD8+ T cells may be involved in the lesional pathology of psoriasis.