火针联合卤米松乳膏治疗稳定期白癜风患者的疗效观察及对CD4+、CD8+、CD4+/CD8+水平的影响

 目的 观察火针联合卤米松乳膏治疗稳定期白癜风的临床疗效，检测对患者CD4⁺、CD8⁺及CD4⁺/CD8⁺水平的影响。方法 选择我院皮肤科及中医科门诊自2018年1月—2019年12月诊治的60例稳定期白癜风患者作为研究对象，随机分成对照组 (30例) 和试验组(30例)，对照组采用卤米松乳膏治疗，试验组予以火针联合卤米松乳膏治疗，比较两组患者治疗前后的白癜风面积评分指数(VASI),观察总有效率以及不良反应发生率。同时检测患者治疗前后CD4⁺、CD8⁺及 CD4⁺/CD8⁺的表达水平。结果两 组患者治疗前的VASI对比无显著差异(P＞0.05)。治疗后，试验组VASI明显低于对照组(9.73±0.56比10.79±1.13，t=4.60,P＜0.05），总有效率明显高于对照组(86.67%比63.33%,X²=4.36,P=0.037）。两组治疗后CD3⁺、CD4⁺、CD4⁺/CD8⁺均高于治疗前，试验组治疗后CD3+为(69.23±5.27)%，CD4⁺ 为(44.03±3.94)%,CD4⁺/CD8⁺比值为 (2.54±0.99)，对照组治疗后CD3⁺为(66.60±7.56)%，CD4⁺为(38.13±6.51)%, CD4⁺/CD8⁺比值为(1.91±0.87)，试验组各指标均高于对照组（均P＜0.05）；治疗后试验组CD8⁺为(19.30±5.55)%，低于对照组的(23.20±8.36)%，差异有统计学意义（P＜0.05）。结论 火针联合卤米松乳膏治疗不仅能有效促进稳定期白癜风患者皮肤恢复正常肤色，提高有效率，且能调节患者T淋巴细胞亚群，提高患者细胞免疫功能。因此火针是一种安全、高效的治疗方法，值得临床推广。     

艾滋病合并肺结核患者治疗前外周血CD4+T淋巴细胞水平、CD4+/CD8+比值与预后的关系

目的 分析艾滋病(AIDS)合并肺结核(pulmonary tuberculosis, PTB)患者治疗前外周血中CD4⁺T淋巴细胞水平、CD4⁺/CD8⁺比值与预后的关系。方法 采用回顾性倾向性评分匹配方法收集长沙市第一医院2018年6月—2020年5月接受治疗且随访1年内生存的37例AIDS合并PTB患者资料，纳入存活组，另以1∶1比例匹配同期接受治疗且随访1年内病死的37例AIDS合并PTB患者资料，纳入病死组；治疗前两组均接受外周血中CD4⁺T淋巴细胞水平、CD4⁺/CD8⁺比值及相关实验室指标检测，重点分析治疗前外周血中CD4⁺T淋巴细胞水平、CD4⁺/CD8⁺比值与AIDS合并PTB患者预后的关系。结果 病死组CD4⁺T淋巴细胞计数、CD4⁺/CD8⁺比值均低于存活组(P<0.05);两组间其他基线资料、实验...     

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。     

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.     

复发性生殖器疱疹患者外周血CD4+CD25+Foxp3+调节性T细胞的检测

目的 研究外周血CD4⁺CD25⁺调节性T细胞(Treg细胞)表型和功能改变所致的细胞免疫抑制效应在复发性生殖器疱疹(RGH)发病机制中的作用.方法 采用免疫荧光标染技术,经流式细胞仪检测34例RGH患者和33例正常人外周血CD4⁺CD25⁺T细胞转录因子Foxp3及细胞毒T细胞相关抗原4(CTLA-4)、糖皮质激素诱导的肿瘤坏死因子受体家族相关基因(GITR)、程序性死亡1(PD-1)等抑制性膜分子的表达水平.同时,用免疫磁珠细胞分选技术从外周血中分选出高纯度的CD4⁺CD25⁺T细胞,经体外刺激后分析胞内分泌白介素10(IL-10)和转化生长因子β(TGF-β)阳性细胞数.结果 RGH患者外周血CD4⁺CD25⁺Foxp3⁺Treg细胞数量比正常人对照组显著增加(P<0.001),CD4⁺CD25⁺T细胞表面抑制性膜分子CTLA-4、GITR、PD-1表达明显增强(P分别<0.001、<0.001及<0.01),胞内IL-10和TGF-β阳性细胞增多(P值分别<0.01及<0.001).结论 单纯疱疹病毒感染可诱导CD4⁺CD25⁺Treg细胞活化增殖,高表达负性共刺激分子和分泌抑制性细胞因子,通过多种机制抑制机体的抗病毒免疫应答.     

滤泡辅助性T细胞CD4+T细胞的表达与子宫内膜异位症伴不孕症患者发病及自身抗体的相关性

目的 探讨滤泡辅助性T细胞(CXCR5⁺)CD4⁺T细胞的表达与子宫内膜异位症伴不孕症患者发病及自身抗体的相关性。方法 选取2017年4月至2020年10月中国人民解放军联勤保障部队第九○一医院诊治的120例子宫内膜异位症伴不孕症患者作为研究对象,设为观察组,进行前瞻性研究。另选取同期120例进行健康体检的志愿者作为对照组。比较两组的CXCR5⁺CD4⁺T细胞表达水平、性激素水平、自身抗体水平,分析CXCR5⁺CD4⁺T细胞表达水平与自身抗体水平的相关性。结果 观察组CXCR5⁺CD4⁺T细胞比例显著高于对照组,差异具有统计学意义(P<0.05);观察组血清抗卵巢抗体(AoAb)、抗精子抗体(AsAb)、抗绒毛膜促性腺激素抗体(HCGAb)、抗心磷脂抗体(AcAb)、抗子宫内膜抗体(EmAb)阳性率均显著高于对照组,差异具有统计学意义(P<0.05);观察组黄体生成素(LH)、睾酮(T)、雌二醇(E<...     

银屑病患者外周血CD4+、CD8+T细胞对角质形成细胞ki67、c-myc及bcl-xL蛋白表达的影响

T细胞按表面标志及功能特征的不同可分为CD4⁺T细胞和CD8⁺T细胞,两者在银屑病发病机制中的作用不尽相同.本研究将CD4⁺T细胞和CD8⁺T细胞分别与角质形成细胞(KC)共培养,探讨了CD4⁺T细胞及CD8⁺T细胞对银屑病患者表皮增值动力学的影响.     

寻常性银屑病患者外周血CD4+CD25+调节性T细胞的检测

调节性T细胞(CD4⁺CD25⁺Treg)是调节性T细胞亚群之一,具有多种独特的特征,包括可识别自身抗原肽、分泌抑制性细胞因子和维持免疫稳态等,在维持机体内环境的稳定、诱导移植耐受以及自身免疫性疾病的发生中发挥作用.     

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.     

中医药对HIV/AIDS抗病毒治疗患者CD4+T淋巴细胞长期变化的影响

目的 探讨中医药治疗对HIV/AIDS患者接受抗病毒治疗后CD4⁺T淋巴细胞计数长期变化趋势的影响。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,回顾性收集2004年参与河南中医项目地区的HIV/AIDS患者的基线信息及随访年的CD4⁺T淋巴细胞计数。按是否参与中医项目分为中医治疗组和非中医治疗组,利用倾向性评分匹配法来控制组间差异,并观察两组患者CD4⁺T淋巴细胞计数的变化趋势。结果 本研究共纳入2 046例HIV/AIDS患者,其中中医治疗组973例,非中医治疗组1 073例,匹配后共得到723对病例,组间差异无统计学意义(P>0.05)。两组CD4⁺T淋巴细胞计数年变化趋势图显示,CD4⁺T淋巴细胞计数<200个/μL和200～350个/μL的HIV/AIDS患者在治疗初期CD4⁺T淋巴细胞计数显著升高,中医治疗组升高得更快。当CD4⁺T淋巴细胞计数达到350个/μL左右时,组间差异消...     

T6+ and HLA-DR+ cell numbers in epidermis of immunosuppressed renal transplant recipients

The increased susceptibility of the skin of chronically immunosuppressed individuals to viral infections and sunlight-induced malignancies suggests specific drug-induced, dysfunction of local immune mechanisms within the sun-exposed skin of these individuals. To help understand the effect of immunosuppressive therapy alone in the absence of ultraviolet light on the immune system of skin, biopsies were collected from non-sun-exposed buttock skin of control, healthy volunteers and kidney transplant recipients immunosuppressed with either azathioprine/prednisone or cyclosporin A/prednisone and examined for incidences of T6+, and HLA-DR+ cells. No significant differences in the incidences of these 2 cell types were found (a) between control individuals and transplants recipients, (b) between transplant recipients receiving either of the immunosuppressive drug regimes, or (c) between transplant recipients who either had or had not developed skin cancer.     

PUVA therapy decreases HLA-DR+ CD1a+ Langerhans cells and epidermal cell antigen-presenting capacity in human skin, but flow cytometrically-sorted residual HLA-DR+ CD1a+Langerhans cells exhibit normal alloantigen-presenting function

We have investigated the effects of PUVA therapy on human Langerhans cell (LC) immunophenotype and function. Epidermal sheets were obtained from exposed, and control shielded, forearm skin at the end of a course of PUVA therapy, in patients receiving treatment routinely for a variety of dermatoses. PUVA therapy decreased the overall number of HLA-DR+CDIa+ LCs in epidermal sheets, and in epidermal cell (EC) suspensions examined using a fluorescence activated cell sorter (FACS). PUVA therapy also reduced the overall EC allostimulatory capacity in the allogeneic epidermal cell-lymphocyte reaction (ELR), and the capacity of ECs to present tetanus toxoid to, and augment concanavalin A-mediated stimulation of, lymphocytes in the autologous ELR. Depressed allostimulation by ECs from PUVA-treated skin could not be restored by indomethacin (added to block prostaglandin synthesis). The reductions in LC numbers and EC allostimulatory capacity varied according to dose, and time since cessation, of PUVA therapy, and in individual patients were of comparable degree. By contrast, the allostimulatory capacity of residual LCs from PUVA-treated skin (purified using the FACS) did not differ from that of purified control LCs. PUVA-induced suppression of cutaneous immune responses, therefore, results at least in part from an overall impairment of EC antigen-presenting capacity. Residual HLA-DR+CDIa+ LCs in PUVA-treated skin which retain their alloantigen-presenting function may represent a subgroup of PUVA-resistant LCs; alternatively, these cells may be as yet unaffected because they have only recently migrated into the epidermis.     

Lack of antagonism to Ni2+ and Co2+ contact allergy from other essential divalent metal ions

The potential antagonistic effects of Ca²⁺, Cu²⁺, Fe²⁺, Mg²⁺, Mn²⁺ and Zn²⁺ on contact allergy to Co²⁺ and Ni²⁺ were studied. The immune response was characterized by the Co²⁺ or Ni²⁺ mediated cellular [methyl-³H]thymidine uptake in peripheral blood mononuclear cell (PBMC) cultures from 6 subjects contact-allergic to Co²⁺ and Ni²⁺ and 6 non-allergic control individuals. Results from the in vitro experiments were further evaluated with Co²⁺-sensitized guinea pigs according to the modified Freund's complete adjuvant test. Ni²⁺ and Co²⁺ (10–50 μM) significantly increased the lymphocyte proliferation in PBMC cultures from contact-allergic subjects in comparison with those from control individuals. Pretreatment of the PBMCs with Ca²⁺, Fe²⁺, Mg²⁺ (10–100 μM) or Mn²⁺ (1–10 μM) did not influence, while Zn²⁺ (100 μM) enhanced, and Cu²⁺ (5 and 10 μM) markedly reduced the Ni²⁺ and Co²⁺ mediated cellular [methyl-³H]thymidine uptake. The inhibition of the Ni²⁺- and Co²⁺-induced cell proliferation by Cu²⁺ in vitro was probably related to toxicity, since the viability of the cells was significantly reduced by applied combinations of Ni²⁺ or Co²⁺ with Cu²⁺. Topical pretreatment of Co²⁺-sensitized guinea pigs with maximum non-irritating doses of CuCl₂· 2H₂O (0.8%) did not affect the challenge testing to CoCl₂· 6H₂O (0.1 and 0.3%). In conclusion, our combined in vitro and in vivo results indicate that Ca²⁺, Cu²⁺, Fe²⁺, Mg²⁺, Mn²⁺ and Zn²⁺ are not able to antagonise the formation of Ni²⁺ and Co²⁺ antigens.     

Roles of CD4+ and CD8+ cells in UVB-induced suppression of splenic alloantigen presenting function

Abstract Whole body ultraviolet light (UV) radiation causes systemic immunosuppression. Splenic antigen-presenting cell (APC) activity is decreased by UV radiation. To determine whether splenic CD4⁺ or CD8⁺ cells are involved in the UV-induced depression of splenic alloantigen presenting function, we investigated the effect of in vivo UV radiation on the splenic stimulatory function in allogeneic mixed lymphocyte reaction in mice after the elimination of CD4⁺ or CD8⁺ cells by administering anti-CD8 or anti-CD4 Ab. Ab-treated and non-treated mice were exposed to UVB radiation (2.5 k.J/m²) twice or eight times. Two exposures to UVB radiation significantly suppressed the splenic alloantigen-presenting function of mice previously treated with anti-CD4 Ab, but hardly affected that of anti-CD8 Ab-treated or non-treated mice 2 days after the last radiation. On the other hand, eight exposures to UVB radiation suppressed this function in all mice. FACS analysis revealed that the UV induced suppression is not associated with a significant decrease in the number of IA⁺ cell, as stimulator cells. It is suggested that CD4⁺ cells are somewhat preventive of the UV-induced depression of splenic alloantigen-presenting function.     

Flow cytometric analysis and sorting of HLA-DR+CD1+ Langerhans cells

There is a considerable need for reliable methods for enumeration and enrichment of Langerhans cells (LCs), since they continue to be the subject of intensive investigation in normal and diseased skin. It has been claimed that standard labelling with either anti-HLA-DR or OKT6 antibodies alone may fail to identify potentially important subsets of LCs with the phenotypes HLA-DR+CD1- and HLA-DR-CD1+. We report here on flow cytometric analysis of suction blister-derived normal epidermal cell (EC) suspensions, double stained with phycoerythrin-conjugated anti-HLA-DR and fluoresceinated OKT6. In seven separate experiments, no evidence for the existence of either HLA-DR+CDI- or HLA-DR-CDI+ ECs was obtained. We found that HLA-DR+CDI+LCs, which constituted a mean of 2.5% (+/- 0.3 SEM) of all ECs, could be readily identified on the basis of fluorescence, and that their light scatter characteristics were those of moderately sized cells of low granularity. We further describe our method for flow cytometric enrichment of such HLA-DR+CDi+ LCs for functional studies, based on selection on both fluorescence and light scatter criteria. Enrichment is to greater than 90% purity, and the method is applicable to the small number of ECs (approximately 1 x 10(6] obtained from a suction blister.     

Oral submucosal dendrocytes: factor XIIIa+ and CD34+ dendritic cell populations in normal tissue and fibrovascular lesions

Factor XIIIa+ and CD34+ dendritic cells, believed to be subsets of monocyte/macrophages, have been identified in dermis and in dermal tumors. The purpose of this study was to determine the presence and distribution of analogous cell types in oral submucosa and oral fibro-vascular lesions. Antibodies to XIIIa, CD34, S-100 protein, and macrophage antigen (MAC 387) were tested on formalin-fixed, paraffin-embedded tissue sections from normal mucosa, peripheral fibroma (PF), peripheral ossifying fibroma (POF), peripheral giant cell granuloma (PGCG), pyogenic granuloma (PG), lymphangioma (La), benign fibrous histiocytoma (BFH), idiopathic histiocytosis (IH), angiofibroma (Af) using an ABC immunoperoxidase technique. Numbers of positively stained cells were compared to unstained cells in the tumors. XIIIa positive submucosal dendrocytes (CD34-, S-100-, MAC 387-) were found in abundance in normal tissue in characteristic distributions: collagen-associated, vessel-associated, and lymphoid-associated. The percentage of XIIIa+ cells in the oral tumors was as follows: PF: 10-30%, POF: 5-10%, PGCG: 0-5%, PG: 5-20%, La: 0%, BFH: 5-25%, IH: 0%, and Af: 10-20%. CD34+ dendrocytes (XIIIa-, S-100-, MAC 387-) were few in number and were found in deeper submucosa, especially around skeletal muscle. Other than blood vascular endothelium, CD34+ cells were not generally seen in the oral tumors studied. It is concluded that two previously unrecognized dendrocyte populations reside in normal submucosa. XIIIa+ cells participate in the formation of some oral reactive and neoplastic lesions.     

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.     

Pathobiology of CD30+ cutaneous T-cell lymphomas

Abstract:  CD30+ cutaneous lymphoproliferative disorders include lymphomatoid papulosis (LyP) and anaplastic large cell lymphoma (ALCL). LyP is associated with development of lymphoma in nearly 20% of patients. Herein is reviewed the clonal relationship of LyP to malignant lymphoma, the concept of a common stem cell for LyP and associated lymphomas, and the role of genetic instability in lymphomagenesis. The possible role of the CD30+ cell as a regulatory T‐cell is introduced and a model for progression of LyP to ALCL is illustrated.