HPV亚型T淋巴细胞亚群和尖锐湿疣复发关系的研究

选择CA患者161例。应用流式细胞仪，检测患者外周血CD3^＋、CD4^＋、CD8^＋T淋巴细胞数，计算CD4^＋／CD8^＋比值；愈后随访1年，观察患者是否复发。比较高危型和低危型之间T淋巴细胞亚群分布和复发率的差异。结果：161例患者HPV6／11型感染占73．91％（复发率31．93％），HPV16／18型感染占9．32％（复发率55．3％），复合型感染占16．77％（复发率51．85％）。各型患者CD3^＋T淋巴细胞总数正常，CD4^＋T淋巴细胞减少，CD8^＋T淋巴细胞正常，CD4^＋／CD8^＋降低，各型间无显著差异。高危型HPV16／18感染和复合型感染复发率高于低危型HPV6／11感染；HPV6、11、16、18以及复合感染都引起CD4^＋T淋巴细胞减少和CD^＋／CD8^＋下降；低危型感染和高危型以及复合型感染对T淋巴细胞亚群分布的影响相似。     

应用流式细胞仪研究深圳地区健康成人及HIV/AIDS患者的免疫状况

目的：研究深圳地区健康人、HIV无症状感染者及AIDS患者的免疫状态，以了解艾滋病早期T细胞亚群的变化过程。方法：应用流式细胞仪三色荧光单克隆抗体（CD4－FITC／CD8－PE／CD3－PC5）检测34例正常健康成人，12例HIV感染无症状者，23例AIDS患者的外周血CD4^ 、CD8 ^ T淋巴细胞计数及CD4^ /CD8^ 比值。结果：HIV感染无症状者及AIDS患者的CD4^ 淋巴细胞及CD4^ /CD8比值均明显低于健康成人（P＜0．01）；HIV感染无症状者CD8^ T淋巴细胞明显高于正常健康人和AIDS患者（P＜0．01）；CD4^ T淋巴细胞随病程进展不断下降，AIDS患者与HIV感染无症状者之间存在着显著差异。结论：T淋巴细胞免疫状况可作为评价AIDS病程进展程度的重要指标。     

儿童面中部NK/T细胞淋巴瘤合并曲霉感染1例

报告儿童面中部NK/T细胞淋巴瘤合并曲霉感染1例。患儿女，8岁，左鼻部皮损6个月，伴发热、左面部肿胀5个月。检查见左务翼组织表面有污褐色痂，周围糜烂，有脓性分泌物，并有异味，周围组织水肿，口腔黏膜有溃疡及坏死。肝脾大。末梢血全血细胞降低。创面镜检邮大量分隔菌丝，经培养鉴定为曲霉菌属。组织病理检查真皮至皮下脂肪有密集的淋巴细胞浸润。真皮血管周围有散在异形的淋巴细胞，皮下脂肪层有吞噬红细胞的组织细胞。免疫组化染色示CD45RO（ ），散在CD56（ ）。PAS染色可见菌丝和孢子。     

特发性CD4^＋T淋巴细胞减少症研究进展

持发性CD4^ T淋巴细胞减少症又称人类免疫缺陷病毒阴性艾滋病样综合征。患者主要特点为CD4^ T淋巴细胞减少，具有与艾滋病相似的临床表现，但又无人类免疫缺陷病毒感染的证据。发病机制主要与T淋巴细胞增生异常、凋亡增强及表面受体功能改变有关。除积极治疗各种机会感染外，最根本的治疗是重建免疫功能。     

扁平苔藓患者外周血T淋巴细胞亚群的检测

应用流式细胞术对29例扁平苔藓患者外周血T淋巴细胞亚群CD4^＋、CD8^＋及CD25^＋进行检测分析。结果：扁平苔藓患者外周血T淋巴细胞亚群CD8^＋明显升高，CD4^＋／CD8^＋、CD25^＋均明显降低，与健康对照组比较有显著性差异（P〈0．05）。提示扁平苔藓患者存在细胞免疫功能紊乱。     

隐球菌性脑膜炎患者临床免疫指标分析

目的：研究隐球菌性脑膜炎（隐脑）患者细胞和体液免疫功能，方法：用液式细胞仪和免疫扩散法检测了12例隐脑患者外周T细胞亚群、NK细胞百分率及体液免疫指标。结果：与正常对照组相比，隐脑患者CD4^ 细胞百分率、CD4^ ／CD8^ 及C3均显著下降（P＜0.01），血清中IgG下降（P＜0.05）。结论：在非获得性免疫缺陷综合症（AIDS）隐脑患者同样存在着细胞免疫低下情况。     

皮肤隐球菌病——口服氟康唑治疗

本文报告了用氟康唑(fluconazole)治疗1例原发性皮肤隐球菌病的结果。患者男性,85岁,左手背外伤继而发展为溃疡3个月。曾用抗菌敷料外敷,但皮损逐渐扩大,疼痛明显。1个月来左前臂又出现了2个触疼性结节。患者因风湿性多发性肌痛,4年来服用强的松龙10mg/d。检查:左手背有5×4cm不规则形状溃疡,周边呈“滚边状”,左前臂伸侧有2个坚实活动的皮下结节,约3cm大小。溃疡及结节部病理示真皮中有大量组织细胞及一些浆细胞和淋巴细胞。组织细胞胞浆中有多数PAS阳性、环六甲基四胺银染色阳性的孢子。组     

糖皮质激素对SLE患者CD4＋、CD8＋T细胞Caspase-3及TRAIL受体基因表达的影响

目的探讨糖皮质激素对系统性红斑狼疮（SLE）患者CD4^＋．CD8^＋T淋巴细胞Caspase-3及肿瘤坏死因子相关凋亡诱导配体（TRAIL）受体基因表达的影响。方法免疫磁珠法分离20例糖皮质激素治疗前后SLE患者及10例正常人对照的外周血CD4^＋,CD8^＋T淋巴细胞，半定量逆转录聚合酶链反应（RT-PCR）分析其Caspase-3及TRAIL受体mRNA的表达。结果SLE患者治疗后CD4^＋T淋巴细胞TRAIL-R1表达显著降低（P〈0．05）；SLE患者治疗前后CD8^＋T细胞Caspase-3的表达显著高于正常人对照（P值分别〈0．01和〈0．05）；SLE患者治疗前CD8^＋T细胞TRAIL-R2的表达显著高于正常人对照（P〈0．05）。结论通过调节SLE患者T细胞TRAIL受体表达以抑制其凋亡可能是糖皮质激素治疗SLE的机制之一。     

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。     

霉康唑治愈一例原发性皮肤隐球菌病

隐球菌病大部分原发于肺部,常常播及脑膜和脑实质.播散性隐球菌病偶可累及皮肤.原发性皮肤隐球菌病是指皮肤损害是其唯一的表现,而无系统性或脑脊液的侵犯.本病较为罕见,可以在含有新型隐球菌的异物损伤皮下以后而出现.作者报告一例男性患者,81岁,因左前臂红肿痛一个月而就诊.查局部红肿湿润,渗出少量脓液,近卫淋巴结不大.给予红霉素治疗无效,且损害继续扩大,以至形成10×6.5cm溃疡.检查肺、神经系统及其他系统无异常.溃疡区活检表现为慢性炎症,可见多数淋巴细胞、组织细胞和少数多形核白细胞浸润.有多数胶样厚荚膜孢子,偶见巨细胞.溃疡组织在沙氏葡萄糖琼脂培养为新型隐球菌生长.此时作痰、尿、脑脊液直接镜检和培养均为阴性.遂     

CD4+ T lymphocytopenia with disseminated HPV

BACKGROUND: There have been several reports of HIV-negative patients with chronic idiopathic CD4+ T lymphocytopenia, the diagnostic criteria for which are: depressed numbers of circulating T lymphocytes (less than 300/ micro l or less than 20%) on more than one occasion; no laboratory evidence of HIV-1 or HIV-2 infection; and the absence of any defined immunodeficiency or therapy associated with depressed levels of CD4+ T lymphocytes. METHODS: We report a patient with disseminated human papillomavirus infection associated with idiopathic CD4+ T-cell lymphocytopenia. A 50-year-old woman presented to the dermatology clinic with a 10-year history of widespread verrucae involving the skin and the cervix. RESULTS: Biopsy from the arm revealed a common wart. PCR analysis performed from the paraffin-embedded block was strongly positive for HPV type 2. Other HPV types (including EV-associated HPV 5, 8, 14, 15, 17) were not found. Further laboratory work up revealed T-cell lymphocytopenia, with an absolute CD4 count of 21. HIV tests were repeatedly negative. She was treated with interferon A 8 million units SQ three times per week with partial improvement. The patient underwent a hysterectomy for cervical dysplasia and a vulvectomy for vulvar intraepithelial neoplasia. She developed small-cell lung carcinoma and died. CONCLUSIONS: The diagnosis of idiopathic CD4+ T-cell lymphocytopenia should be considered in any patient with widespread viral, fungal, or mycobacterial infection whose HIV test is negative, and appropriate evaluation of the absolute CD4+ counts should be performed.     

Cutaneous infections by papillomavirus, herpes zoster and Candida albicans as the only manifestation of idiopathic CD4+ T lymphocytopenia

BACKGROUND: Selective depletion of CD4+ T lymphocytes is common in both primary and secondary immunodeficiencies. Idiopathic CD4+ T lymphocytopenia (ICL) cases are defined as a persistent CD4+ T lymphocyte count of less than 300x10(6) cells/L and/or less than 20% of the total T-cell count. METHOD: A 40-year-old woman, with a history of psoriasis and paracetamol allergy, presented with persistent warts of the hands and condylomas of the ano-genitalia. Histological and virological analysis was carried out on genital and cutaneous lesions and peripheral blood. RESULTS: Serology for HIV-1, HIV-2, Epstein-Barr virus and parvovirus B19 were negative. There was lymphopenia of 10% CD4+ cells, with normal numbers of total leukocytes; there were no other-abnormal immunological findings. DNA analysis of cutaneous lesions revealed HPV-49 and HPV-3 in the hands and HPV-6 in the genital region. CONCLUSIONS: The cause of the ICL in this patient is unknown. HPV is not known to be an immunosuppressive agent; it remains to be determined whether the HPV-associated lesions are the cause or the result of immunosuppression.     

Idiopathic CD4+ T lymphocytopenia associated with disseminated flat warts and alopecia areata

Idiopathic CD4+ T lymphocytopenia is a very rare condition characterized by persistent depletion of circulating CD4+ T lymphocytes, without evidence of HIV or HTLV infection, or other identifiable causes of immunodeficiency. The syndrome can present with dermatological diseases, including viral, fungal and bacterial infections, as well as Kaposi's sarcoma, epithelial cell malignancies, lymphoma and inflammatory dermatoses. We report the case of a 47-year-old woman with idiopathic CD4+ T lymphocytopenia who presented with a 10-year history of disseminated and refractory flat warts from which human papillomavirus type 3 DNA was identified. The patient also had alopecia areata.     

Isolated human papillomavirus 18-positive extragenital bowenoid papulosis and idiopathic CD4+ lymphocytopenia

We report a case of isolated extragenital bowenoid papulosis (BP) in a young man with an idiopathic low CD4 count. The lesions occurred on the dorsal aspect of his left middle finger and were not associated with genital involvement. Polymerase chain reaction studies of a biopsy demonstrated human papillomavirus 18. As far as we are aware, this is the first documented case of BP (genital or extragenital) associated with idiopathic CD4 lymphocytopenia.     

HIV-1 RNA有效抑制下T淋巴细胞与HAART持续治疗时间的相关性

目的观察HIV-1RNA有效抑制下HAART持续治疗时间与T淋巴细胞的相关性。方法对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患者进行回顾性研究,采用Spearman秩和相关检验考察HAART持续治疗时间与CD4+,CD3+,CD8+,CD4+CD28+,CD4+CD45RA+,CD4+CD45RO+和CD8+CD38+,CD38+T细胞的相关性。同时根据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)4组,考察4组间T细胞亚群的差别。结果 HIV-1RNA有效抑制下HAART持续治疗时间与CD4+CD28+,CD4+CD45RA+,CD4+CD45RO+T细胞绝对计数呈正相关,相关系数r分别为0.214,0.249,0.259,P值分别为0.007,0.016,0.012。HAART持续治疗时间分别与CD8+CD38+,CD3+,CD8+T细胞表达比例呈负相关,r分别为-0.352,-0.204,-0.236,P值分别为0.000,0.041,0.018;与CD28+细胞绝对计数呈正相关(r=0.204,P=0.042)。CD4+T细胞绝对计数与CD4+CD28+,CD4+CD45RO+T细胞相对计数呈正相关,r分别为0.421,0.241,P值分别为0.000,0.015;与CD8+CD38+T细胞相对计数呈负相关(r=-0.268,P=0.007)。D组的CD4+CD28+T细胞绝对计数显著高于A组(P<0.05);C,D组的CD4+CD45RA+T细胞绝对计数显著高于A组(P<0.05)。D组的CD8+CD38+T细胞相对计数(17±9)显著低于A组(25±8)(P<0.05)。结论 AIDS患者经过HAART治疗病毒复制被抑制后,HAART持续治疗时间与某些T细胞亚群数量有关,HAART持续治疗时间是AIDS患者免疫重建的因素之一。     

Active psoriasis and profound CD4+ lymphocytopenia

We report the case of a patient with a long-standing history of widespread chronic plaque psoriasis, who was recently found to have a profound CD4⁺ lymphocytopenia. He is human immunodeficiency virus (HIV) negative. His psoriasis remains active and widespread, and he has had 60 cutaneous malignancies, including many squamous cell carcinomas, excised over the last 10 years. In the past he has had numerous cutaneous viral warts. Despite a low peripheral blood CD4⁺ T-cell count, similar numbers of activated T cells, identified by double labelling for CD4 and HLA-DR antigens, were found in the epidermis of our patient as other individuals with psoriasis. Thus, there appear to be sufficient activated CD4⁺ T cells in our patient's psoriatic plaques to maintain the psoriatic process.     

血热型/血燥型银屑病患者外周血T淋巴细胞亚群变化

目的 探讨血热型/血燥型银屑病患者外周血T淋巴细胞亚群变化规律,并和正常人作比较.方法 选择血热型银屑病患者35例、血燥型银屑病患者30例和正常人36例的外周血单一核细胞,采用流式细胞分析方法检测T淋巴细胞亚群中CD4⁺和CD8⁺的比例.结果 在银屑病患者外周血中,血热CD4M⁺淋巴细胞明显低于血燥型或正常人,CD8⁺淋巴细胞明显高于血燥型或正常人,CD4⁺/CD8⁺比值明显倒置,而血燥型CD4⁺和CD8⁺淋巴细胞与正常人相比没有差异.结论 T淋巴细胞变化可能是血热型/血燥型银屑病辨证求因的主要效应细胞之一.     

银屑病患者体外系统血液固有免疫反应中CD4~+ CD25~+ T细胞及CD4~+ CD25~(high) T细胞的变化与意义

目的用体外系统血液固有免疫反应体系研究银屑病患者外周血CD4+ CD25+T细胞及CD4+ CD25highT细胞的变化,并探讨其在银屑病发病机制中的作用。方法将灭活大肠杆菌悬液(3×108/mL)0.2mL作为免疫原激活剂加入枸橼酸抗凝的全血细胞悬液0.2mL和血浆0.3mL中,37℃水浴1h,用流式细胞仪测定CD4+ CD25+T细胞及CD4+ CD25highT细胞的比例。结果在加入大肠杆菌的银屑病全血细胞组(银屑病实验组)CD4+ CD25highT细胞比例(1.88%)明显高于银屑病对照组(1.41%)(P﹤0.01),CD4+ CD25+T细胞及CD4+ CD25highT细胞的比例(16.86%,1.88%)明显低于加入大肠杆菌的健康实验组(24.26%,2.81%)(P﹤0.01);银屑病对照组CD4+ CD25+T细胞及CD4+ CD25highT细胞的比例(15.97%,1.41%)较健康对照组明显降低(21.75%,2.17%)(P﹤0.01);健康实验组CD4+ CD25+T细胞及CD4+ CD25highT细胞的比例群(24.26%,2.81%)均明显高于健康对照组(21.75%,2.17%),(P﹤0.05)。结论银屑病患者CD4+ CD25+T细胞及CD4+ CD25highT细胞比例降低,外来抗原刺激后比例升高,但与健康正常人存在差异。这可能与其复杂的系统免疫学发病机制相关。     

神经梅毒合并HIV阳性患者的脑脊液及血液指标分析

目的：探讨脑脊液实验室检测在神经梅毒合并HIV阳性患者中的诊断价值及血清快速血浆反应素试验（rapid plasma reagent test, RPR）滴度、CD4+T细胞计数在神经梅毒腰穿指征中的应用。方法：收集2015年1月至2019年12月就诊于北京佑安医院的梅毒合并HIV阳性患者106例,采集脑脊液(cerebrospinal fluid, CSF)进行脑脊液白细胞（CSF-WBC）、脑脊液蛋白（CSF-protein）及脑脊液梅毒螺旋体颗粒凝集试验(treponema pallidum particle assay, TPPA)、RPR滴度检测,采集血液进行RPR滴度、CD4+T细胞计数检测,根据神经梅毒的诊断分神经梅毒组和非神经梅毒组,对两组的脑脊液检测结果、血清RPR滴度及CD4+T细胞计数检测结果进行分析。结果：106例梅毒合并HIV阳性患者中神经梅毒发病率为33.02%,CSF-RPR及CSF-TPPA对HIV阳性梅毒患者发生神经梅毒的诊断敏感性为68.57％和97.14％,特异性为92.96％和49.29％;CSF-WBC和CSF-protein的ROC（受试者工作特征曲线）分析曲线下面积（area under curve, AUC）分别为0.911和0.913,CSF-WBC为10.5/μL、CSF-protein为272.15 mg/L时,约登指数最大;血清RPR≥1∶16患者发生神经梅毒的几率是血清RPR<1∶16患者的1.52倍（OR 1.52,CI 1.14～2.04,P<0.05）,CD4+T细胞≤350个/μL发生神经梅毒的几率为CD4+ T细胞>350个/μL患者的2.37倍（OR 2.37, 95％ CI 1.64～3.41,P<0.05）。结论：HIV阳性患者神经梅毒的发病率较高,CSF-RPR对HIV阳性患者发生神经梅毒具有较高的诊断价值,血清RPR滴度≥1∶16和CD4+T≤350个/μL,是HIV阳性患者神经梅毒的危险因素。