高效抗逆转录病毒疗法治疗HIV-1感染者的免疫学变化

目的 探讨高效抗逆转录病毒疗法(HAART)对人免疫缺陷病毒1型(HIV-1)感染者免疫重建和部分免疫激活标志变化的影响。方法 37例HIV-1感染者,经两种核苷类逆转录酶抑制剂和一种非核苷类逆转录酶抑制剂组方的HAART一年治疗,分别在治疗前、治疗12周、24周和48周,检测其血浆HIV-1病毒载量、CD3⁺CD4⁺、CD3⁺CD8⁺、CD4⁺CD45RA⁺CD62L⁺、CD4⁺CD45RO⁺、CD8⁺CD38⁺、CD4⁺CD28⁺、CD8⁺CD28⁺细胞数和血浆可溶性的CD27(sCD27)分子水平。结果 HIV-1病毒载量的变化与CD3⁺CD4⁺淋巴细胞计数、CD4⁺CD28⁺、CD8⁺CD28⁺细胞计数和百分比呈明显的负相关关系;与CD8⁺CD38⁺细胞计数和百分比、sCD27水平呈明显的正相关关系。抗病毒效果好的完全应答组上述各项检测指标比抗病毒效果差的部分应答组显示出更显著的变化。结论 CD8⁺CD38⁺、CD4⁺CD28⁺、CD8⁺CD28⁺细胞计数和百分比以及sCD27水平与病毒载量在HAART治疗中显示同步变化,是观察抗病毒效果和免疫学效果的指标。     

高效抗逆转录病毒疗法(HAART)对HIV/AIDS患者免疫功能的影响

目的评价高效抗逆转录病毒疗法(highly active antiretroviral therapy,HAART)对HIV/AIDS患者的疗效。方法采用HAART治疗73例HIV/AIDS患者,流式细胞仪测定治疗前后HIV/AIDS患者体内CD4+,CD8+T淋巴细胞数量,定量ELISA法检测血浆细胞因子IL-2,IL-10和TGF-β1水平。结果经HAART治疗后,CD4+T细胞数量显著回升(P(0.01),但CD8+T细胞变化不大(P(0.05)。血浆IL-10水平较治疗前明显下降(P(0.05),IL-2水平较治疗前升高(P(0.05),TGF-β1的水平显著降低(P(0.01)。结论HAART治疗HIV/AIDS患者疗效显著,对于重建免疫功能、改善体内细胞因子失调有明显效果。     

多发性肌炎和皮肌炎外周血CD45RA+及CD45RO+细胞亚群的变化

目的: 研究多发性肌炎(PM)和皮肌炎(DM)外周血单一核细胞(PBMCs)中CD45RA+、CD45RO+细胞亚群的变化.方法: 应用双色荧光标记抗体、流式细胞仪对PM和DM外周血CD45RA+、CD45RO+细胞亚群进行了检测.结果: (1)PM和DM的PBMCs中CD45RA+细胞显著低于对照组,CD45RO+细胞和CD45RO+/RA+比值均显著高于对照组,PM的CD45RA+细胞显著低于DM(均P＜0.05).(2)在PM的CD4+亚群中,CD45RA+细胞显著低于对照组和DM,CD45RO+细胞和CD45RO+/RA+比值显著高于对照组(均P＜0.05).(3)在DM的CD4+亚群中,CD45RA+细胞与对照组比较无显著性差异(P＞0.05),CD45RO+细胞和CD45RO+/RA+比值显著高于对照组(均P＜0.05).(4)在CD8+亚群中,PM和DM的CD45RA+、CD45RO+细胞与对照组比较,均无显著性差异(均P＞0.05),但CD45RO+/RA+比值均显著高于对照组(均P＜0.05).结论: 在PM和DM自身免疫发病过程中PBMCs和CD4+、CD8+亚群中的CD45RO+、CD45RA+细胞可能起重要作用,PM和DM在免疫学方面存在一定的异质性.     

免疫缺陷性皮肤病

20121534 HIV-1RNA有效抑制下T淋巴细胞与HAART持续治疗时间的相关性/温敏(云南省中研院),李艳萍,江涛…∥中国皮肤性病学杂志.-2012,26(2).-95～98对102例HAART持续治疗时间超过6个月,血浆HIV-1RNA<50个拷贝/mL的AIDS患者进行回顾性分析。根据HAART持续治疗时间将102例AIDS患者分为A(6～12个月),B(13～24个月),C(25～36个月),D(37～52个月)四个组,分析四组间T细胞亚群的差异。结果:HIV-1RNA有效抑制下HAART持续治     

未治疗HIV/AIDS中CD4~+T淋巴细胞计数与机会性感染的相关性分析

目的探讨未抗病毒治疗HIV感染者/艾滋病病人(HIV/AIDS)CD4~+T淋巴细胞计数及其自然变化与机会性感染(OIs)1年内发生率之间的关联,为临床防治OIs提供依据。方法对新报告的739例HIV/AIDS开展为期1年、每3个月一次随访的队列研究,了解其1年内OIs出现情况,获取OIs出现与未出现者基线与末次CD4~+,CD8~+T淋巴细胞计数数据,描述并比较其末次与基线T淋巴细胞计数自然变化速率。结果 739例研究对象中207例(28.01%)1年内出现OIs,50岁及以上年龄组1年内OIs发生率(79.69%)较50岁以下年龄组(23.11%)高(P0.05),随着基线CD4~+T淋巴细胞计数的降低,1年内OIs发生率由8.97%上升至69.02%(P0.05);OIs各组的CD4~+,CD8~+T淋巴细胞计数值及CD4/CD8比值均显著低于无OIs组(P0.05);CD4~+T淋巴细胞计数快速、平缓下降组OIs出现构成比分别为48.72%和25.18%,而CD4~+T淋巴细胞计数平缓、快速上升组OIs出现构成比分别为18.45%和9.01%,差异有统计学意义(P0.05)。结论 CD4~+T淋巴细胞计数水平越低OIs增加越明显,无论基线CD4~+T淋巴细胞计数水平是高是低,CD4~+T淋巴细胞计数快速下降均对应着OIs出现几率的明显提高,CD4~+T淋巴细胞计数水平及其下降速率对OIs发生的预测、预防有重要的指导意义。     

河南某地女性HIV/AIDS患者高脂血症及影响因素分析

目的探讨女性HIV感染者/AIDS患者(HIV/AIDS)高脂血症患病率及其影响因素,为临床提前干预提供依据。方法以"艾滋病综合防治数据信息系统"和"中医药治疗艾滋病数据库"为数据来源,收集河南中医项目地区2018年女性HIV/AIDS患者相关信息,利用SPSS软件,采用Logistic回归方法分析女性HIV/AIDS患者高脂血症的影响因素。结果共纳入1 538例女性HIV/AIDS患者,平均年龄(49.36±8.84)岁,其中高脂血症414例(26.92%),HIV确诊时间10年(OR=0.363,95%CI:0.174～0.756)、含LPV/r HAART方案(OR=1.522,95%CI:1.161～1.997)、HAART治疗10年(OR=3.139,95%CI:1.548～6.367)、肝功能损伤(OR=1.676,95%CI:1.196～2.35)、血糖升高(OR=2.075,95%CI:1.507～2.856)、CD4~+细胞计数350～500个/mL(OR=2.27,95%CI:1.223～4.212)、CD4~+细胞计数500个/mL(OR=3.139,95%CI:1.727～5.704)、服用中药(OR=1.463,95%CI:1.086～1.972)均是高脂血症的危险因素。结论 HIV感染病程的延长、HAART服药时间的延长、含LPV/r HAART方案、肝损伤、血糖升高、CD4~+细胞计数升高、服用中药均是高脂血症的危险因素,其中CD4~+细胞计数与高脂血症呈正相关,应提前进行预防干预。     

高效抗逆转录病毒治疗对艾滋病患者外周血淋巴细胞亚群的影响

目的:探讨HAART治疗对AIDS患者外周血淋巴细胞亚群的影响。方法:选取我院近期收治的AIDS患者90例,分为A、B、C三组,并分别于治疗前、治疗后3个月,6个月,12个月及24个月进行血浆病毒载量和外周血T淋巴细胞CD4+亚群水平检测,分析外周血淋巴细胞CD4+亚群动态变化情况。结果:治疗前A组患者T淋巴细胞CD4+亚群水平显著高于B组和C组(P0.05);治疗后3个月B组患者T淋巴细胞CD4+亚群水平显著低于C组(P0.05);治疗后6个月B组患者T淋巴细胞CD4+亚群水平显著低于A组和C组(P0.05);治疗后12个月B组患者T淋巴细胞CD4+亚群水平显著低于C组(P0.05);治疗后24个月C组患者T淋巴细胞CD4+亚群水平显著高于A组和B组(P0.05);A组患者治疗前T淋巴细胞CD4+/CD28+亚群水平显著高于B、C组(P0.05);三组患者治疗后3、6、12及24个月T淋巴细胞CD4+/CD28+亚群水平比较差异无统计学意义(P0.05)。结论:HAART治疗有助于恢复AIDS患者T细胞免疫功能,,这与CD4+T淋巴细胞亚群水平动态变化密切相关。     

HIV感染者中CD8~+T淋巴细胞及发展为AIDS的观察

CD8~+T淋巴细胞增多是HIV-1感染者和AIDS病人的早期免疫学异常表现之一,但对于这种细胞计数增加的意义尚存在有不同的看法。作者应用临床流行病学方法对血清HIV-1阳性者进行了前瞻性研究。方法:研究对象为340例血清HIV-1阳性的男性病人,通过门诊、电话随访和每年的全国死亡登记掌握其病情发展为AIDS和死亡等状况。用流式细胞仪分析CD4~+、CD 8~+T淋巴细胞,并作白细胞总数和分类。连续观察60个月,分别研究CD4~+及CD8~+细胞计数的初始水平、动态变化与发展成为AIDS     

CD8~+T淋巴细胞各亚群与HIV感染疾病进程的关系

目的探讨CD8+T淋巴细胞各亚群在HIV感染性疾病发病中的作用。方法应用流式细胞仪荧光染色技术检测HIV/AIDS患者Ⅱ期25例、Ⅲ期17例和26名健康体检人员外周血CD8+/CD28+T,CD8+/CD38+T,CD8+/CD95+T,CD8+/HLA-DR+T淋巴细胞表达,并用RT-PCR检测HIV/AIDS患者血清HIV-RNA载量。结果 CD8+/CD38+T和CD8+/HLA-DR+T细胞在健康对照组、HIV/AIDS患者Ⅱ期、Ⅲ期中差异均有统计学意义(P0.01),并都与HIV-RNA载量存在正相关(r=0.480,P0.01;r=0.455,P0.01);Ⅱ期、Ⅲ期患者中,CD8+/CD95+T细胞高于健康对照组,差异有统计学意义(P0.01);Ⅱ期患者和健康对照组中,CD8+/CD28+T细胞均高于Ⅲ期患者(P0.01)。结论 CD8+/CD38+T,CD8+/HLA-DR+T淋巴细胞亚群与HIV感染疾病进展显著相关,并参与患者免疫活化的调节。     

HIV/AIDS患者CD4~+ T细胞中CD25和CD8~+ T细胞中CD28的表达

目的探讨外周血CD4+ T细胞中CD25表达率和CD8+ T细胞中CD28表达率在HIV/AIDS患者发病中的作用。方法应用流式细胞仪荧光染色技术检测35例HIV/AIDS患者CD4+ T细胞中CD25表达和CD8+ T细胞中CD28的表达,以41名健康体检人员做对照。结果HIV/AIDS患者和健康对照组之间CD4+ T细胞中CD25表达率(27.51±4.23)%,(44.41±9.17)%,CD4+25+ T细胞占淋巴细胞的比例(2.00±1.42)%,(16.62±4.60)%,CD4+25- T细胞占淋巴细胞的比例(5.16±3.37)%,(21.03±6.19)%,CD8+ T细胞中CD28中的表达率(25.12±6.33)%,(44.24±8.61)%,CD8+28- T细胞占淋巴细胞的比例(36.85±8.98)%,(13.33±4.58)%的差异均有显著性(P<0.01),CD8+ 28+ T细胞占淋巴细胞的比例(12.31±4.14)%,(10.51±3.71)%差异无显著性(P>0.05)。结论HIV/AIDS患者CD25在CD4+ T细胞与CD28在CD8+ T细胞的表达率降低可能与HIV感染后引起的免疫缺陷有关,CD8+ CD28- T细胞的增加有助于促进HIV/AIDS患者的炎性反应和免疫激活。     

Identification of lesional CD4+ CD25+ Foxp3+ regulatory T cells in Psoriasis

BACKGROUND: Depletion of CD4+ CD25+ Foxp3+ naturally occurring regulatory T cells (T(reg)) induces autoimmune phenomena. These cells have not yet been fully characterized in the skin of psoriatic patients. OBJECTIVES: To prove that the Zenon immunofluorescent labeling technique is suitable for the demonstration of co-localization of T-cell markers and in particular to show the distribution of T(reg) in psoriatic skin. METHODS: In biopsies derived from normal and psoriatic skin, CD4+ CD25+, CD4+ CD45RO+, CD8+ CD25+, CD8+ CD45RO+ and CD4+ CD25+ Foxp3+ cells in the dermis and in the epidermis were immunophenotyped, using a quantitative immunofluorescent labeling technique (Zenon), analyzed and compared using image analysis. RESULTS: The immunofluorescent labeling technique was shown to be an easy and reliable tool to demonstrate co-localization of T-cell markers. In psoriasis, all pathogenic T-cell subsets (CD4+ CD25+, CD4+ CD45RO+, CD8+ CD25+ and CD8+ CD45RO+ cells) were significantly increased in the dermis and in the epidermis, as compared to normal skin (all p < 0.05). Using this labeling technique we were able to reveal CD4+ CD25+ Foxp3+ T(reg) in psoriatic dermis, but not in the dermis of normal skin (p < 0.0001). CONCLUSIONS: The Zenon immunofluorescence technique in combination with image analysis is suitable for the demonstration of co-localization of T-cell markers in tissue. Increased numbers of pathogenic T cells (CD4+ CD25+, CD4+ CD45RO+, CD8+ CD25+ and CD8+ CD45RO+) were shown in the dermis and epidermis, whereas CD4+ CD25+ Foxp3+ T(reg) were identified in psoriatic skin with a predilection for the upper dermis.     

Immune reconstitution in HIV-1 infected subjects treated with potent antiretroviral therapy

The introduction of potent antiretroviral drug regimens contributed to a decline in HIV-1 associated morbidity and mortality. Clinical observations of spontaneous remission of previously untreatable opportunistic infections in subjects on highly active antiretroviral therapy (HAART) reflect the substantial degree of immune reconstitution which can be achieved by those therapies. A biphasic increase of CD4+ T lymphocytes has been reported including naive (CD45RA+) and memory (CD45RO+) cell subsets. Proliferative lymphocyte responses to recall antigens and mitogens are enhanced over time, while T lymphocyte activation is largely reduced and T cell receptor (TCR) repertoires are partly restored. Proliferative lymphocyte responses specific to HIV-1 antigens, in contrast, remain weak. A complete normalisation of HIV-1 associated immunological alterations has not been reported so far, but the observation period of subjects on potent antiretroviral therapies is still relatively short.     

Dominance of memory over naive T cells in contact dermatitis is due to differential tissue immigration

CD4+ T cells include a naive (CD4-, CD45RO-, CD29-, CD45RA+) as well as a memory subpopulation (CD4+, CD45RO+, CD29+, CD45RA-). These subpopulations represent different stages in T-cell development and function. Recently, it has been shown that inflammatory and neoplastic CD4+ T-cell infiltrates are dominated by the memory subpopulation, whereas both subpopulations are about the same size in the peripheral blood. This was thought to be the result of in situ maturation of naive into memory T cells. We analysed early positive patch-test reactions 1-2 days after antigen challenge and found that most of the CD4+ T cells that had freshly immigrated into the tissue carried the memory phenotype. Their preferential migration may be mediated by at least five adhesion molecules expressed on their cell surface. This observation has important pathogenetic implications, since memory T cells can be rapidly activated by antigens and secrete a wide variety of pro-inflammatory cytokines.     

Adult T-cell leukemia/lymphoma (ATL) –clinical, histopathological, immunological and immunohistochemical characteristics

Twenty-one patients with ATL were assessed. The predominant physical findings were lymph node and bone marrow involvement, skin involvement, hepatosplenomegaly and leukemic manifestations. The predominant histopathological findings in both skin and lymph node specimens were the diffuse medium-sized cell type and the diffuse mixed cell type. Some phenotypic discrepancy was found between the neoplastic cells in the peripheral blood, lymph nodes and skin of patients with ATL with respect to CD45RA and CD45RO, and CD7, CD29, CD25 and HLA-DR. That is, the predominant neoplastic cell phenotype was the helper T-cell, which was CD3+, CD4+, CD7+, CD25+, CD45RA+ and HLA-DR+, and CD29- and CD45RO- in peripheral blood and lymph nodes, and CD3+, CD4+, CD7+, CD29+, CD45RO+ and HLA-DR+, and CD45RA- in the skin. In other words, we have described the phenotypic heterogeneity of ATL cells and demonstrated the heterogeneity of CD45R isoform expression on ATL cells in different organs--the skin, peripheral blood and lymph nodes--of the same patient.     

Plaque psoriasis vs. atopic dermatitis and lichen planus: a comparison for lesional T-cell subsets, epidermal proliferation and differentiation

BACKGROUND: T-cell infiltration in plaque psoriasis has recently been an important subject of investigation. Interestingly, comparative analyses of the disease-specific composition of the lesional T-cell infiltrate in plaque psoriasis and other inflammatory dermatoses have only sparsely been performed. OBJECTIVES: To compare plaque psoriasis vs. atopic dermatitis and lichen ruber planus with respect to T-cell subsets, epidermal proliferation and keratinization. PATIENTS AND METHODS: Biopsies were taken from untreated lesional skin of patients, six with psoriasis, six with atopic dermatitis and six with lichen planus. T-cell subsets (CD4+, CD8+, CD45RO+, CD45RA+, CD2+, CD25+), an epidermal proliferation (Ki-67) and a keratinization marker (K10) were stained immunohistochemically and quantified using image analysis. RESULTS: The high number of CD8+ T cells (52 +/- 13 cells mm(-1)) found in the psoriatic epidermis was not found in the epidermis of atopic dermatitis (9 +/- 4), nor in the epidermis of lichen planus (34 +/- 10). The other T-cell subsets in the epidermis and dermis showed no statistically significant differences between psoriasis and atopic dermatitis. In contrast to the limited presence of CD4+, CD8+ and CD2+ in the psoriatic dermis (110 +/- 19, 27 +/- 9, 127 +/- 41, cells mm(-1), respectively), more impressive numbers of these cells were observed in the dermis of lichen planus (300 +/- 53, 144 +/- 38, 272 +/- 48, respectively). CD45RO+ memory effector T-cell counts were significantly higher in the epidermis of lichen planus (39 +/- 10) than in psoriasis (19 +/- 5). Psoriatic epidermis proved to have major keratinocyte hyperproliferation (247 +/- 26 cells mm(-1) lamina basalis), as compared with atopic dermatitis (134 +/- 15) and lichen planus (128 +/- 20). Furthermore, a marked decreased expression of keratin 10 was observed in psoriasis (41% of epidermal area) contrary to atopic dermatitis (70%). CONCLUSIONS: Psoriatic epidermis exhibits a pronounced CD8+ epidermotropism with accompanying epidermal hyperproliferation and abnormal keratinization, which changes are only minimally expressed in atopic dermatitis and lichen planus. In plaque psoriasis, substantially fewer activated CD4+ and CD8+ T cells in the dermis and less CD45RO+ T cells in the epidermis are present in comparison with lichen ruber planus.     

T-cell inducer populations in cutaneous inflammation: a predominance of T helper-inducer lymphocytes (THi) in the infiltrate of inflammatory dermatoses

The mononuclear infiltrate found in a variety of inflammatory dermatoses was characterized by a predominance of T helper-inducer lymphocytes (THi), CD4+/CD45RA-/CD45RO+, a population of cells responsible for maintaining and promoting immune reactions. Only small numbers of T-suppressor-inducer lymphocytes (TSi), CD4+/CD45RA+/CD45RO-, cells responsible for inducing CD8 suppressor-effector cells to 'down regulate' immune reactions, were seen. The predominance of CD4+ THi lymphocytes was common to all dermatoses studied and suggests a common final pathway in chronic cutaneous inflammation, irrespective of initial causative factors.     

Primary cutaneous T cell lymphomas: photochemotherapy immunomodulation with analysis of the inflammatory‐expansive cellular dynamic

Primary cutaneous T cell lymphomas (CTCLs) are characterized by hyperproliferation of malignant CD4+ T cells with primary localization on the skin. The common characteristics are the migration of the malignant mature T‐lymphocytes into the epidermis, with hyperproliferation of malignant CD4+ T cells and epidermotropism. Sézary syndrome (SS) is the leukemic variant. It was established that CTCLs arise from a clonal expansion of CD4+ T cells with an identical rearrangement of the T cell receptor. The purpose of this study was to evaluate the immunomodulation effect of photochemotherapy‐A (psoralen plus ultraviolet A (PUVA)). Pre‐ and post‐PUVA punch skin biopsies of nine patients were stained immunohistochemically for CD34+, CD8+, CD7+, CD16+, CD56+, CD1a+, Bcl2+, p53+, CD45RA+, and CD45RO+ cells. The results showed a pre‐PUVA cells/mm² without significant difference among expansive or reactive cells. Post‐PUVA analysis showed a significant decrease in the mean of expansive‐reactive cells. PUVA immunomodulated decreasing cellular infiltrate. These findings could contribute to the comprehension of how PUVA acts. We achieved ectoscopic clearance of the lesions, although post‐PUVA, there still was a mononuclear pathological infiltrate. This result demonstrates that the PUVA treatment should only be withheld when the histological analysis is normal.     

艾滋病合并马尔尼菲青霉病患者二期预防性治疗影响因素的回顾分析

目的 探讨影响艾滋病合并马尔尼菲青霉病（PSM）患者预防PSM复发的二期预防性治疗时间长短的因素。方法 回顾性分析92例广西壮族自治区疾病预防控制中心/无国界门诊确诊的艾滋病合并PSM成人患者,以停用二期预防性治疗时患者血CD4+ T淋巴细胞计数水平为标准,将病例分两组,Ⅰ组在 CD4+ T细胞≥200 × 106/L后、Ⅱ组在100 × 106/L ~ < 200 × 106/L后停用PSM二期预防性治疗,比较两组的疗程和疗效,并分析患者临床脏器累及、合并症、抗真菌方案、抗病毒治疗时机等不同因素对二期预防性治疗时间的影响。运用SPSS 13.0统计软件包完成数据分析。结果 92例患者都得到高效抗逆转录病毒治疗（HAART）,两组患者在性别、年龄、随访时间上差异均无统计学意义（P值均 ＞ 0.05）,在器官累及、合并症、抗真菌治疗方案的构成以及疗效、抗真菌治疗时间的差异均无统计学意义（P均 ＞ 0.05）,但Ⅱ组患者二期预防性治疗时间［（8.13 ± 5.13）个月］较Ⅰ组［（12.44 ± 9.51）个月］短（P < 0.05）。HAART开始于PSM治疗后、合并其他感染、合并结核感染等因素导致二期预防性治疗时间延长,且三者的影响依次从大到小;而HAART开始于PSM治疗前较开始于PSM后二期预防性治疗时间短（P < 0.05）。结论 艾滋病合并PSM患者HAART后,当CD4+ T淋巴细胞恢复到≥100 × 106/L后3 ~ 6个月可以停用二期预防性治疗;影响二期预防性治疗用药时间的积极因素是抗马尔尼菲青霉治疗前开始HAART,负面因素有HAART开始于抗马尔尼菲青霉治疗后、合并其他感染或合并结核感染等。     

Memory effector (CD45RO+) and cytotoxic (CD8+) T cells appear early in the margin zone of spreading psoriatic lesions in contrast to cells expressing natural killer receptors, which appear late

BACKGROUND: An influx of immunocytes, increased epidermal proliferation and abnormal keratinization are hallmarks of the psoriatic lesion. T-lymphocyte subsets in particular activated effector memory T cells and natural killer (NK) T cells have been suggested to play an important role in the pathogenesis of psoriasis. OBJECTIVES: In the present study we investigated the number of T-cell subsets (CD4, CD8, CD45RO, CD45RA, CD2, CD25), cells expressing NK receptors (CD94 and CD161), the proliferation marker Ki67 and the keratinization marker keratin (K10) across the margin of the spreading psoriatic plaque: distant uninvolved skin, the outer margin (immediately outside the clinical edge), the inner margin (immediately inside the clinical edge) and the central area. PATIENTS AND METHODS: Eight patients with active psoriasis vulgaris participated in this study. Biopsies were taken from the spreading psoriatic lesion from the distant uninvolved skin, the outer margin, the inner margin and the central area. Biopsies were processed for immunohistochemical staining. RESULTS: In the outer margin CD8+ (cytotoxic T cells) and CD45RO+ (memory effector T cells) T lymphocytes invade the epidermis and in this early stage the activation markers CD2 and CD25 also show a substantial increase. The next phase, from the outer to the inner margin, shows a statistically significant increase of these markers, and especially, the cells expressing NK receptors (CD94 and CD161) show a massive increase together with a significant increase of epidermal proliferation (Ki67) and a decrease of the K10+ epidermal surface. CONCLUSIONS: CD8+, CD45RO+, CD2+ and CD25+ T cells have a role in the early phase of the psoriatic process, whereas CD94- and CD161-expressing cells together with epidermal proliferation and keratinization are involved in a later phase.