病毒性肝炎患者外周血T细胞亚群的变化

<正> 应用APAAP桥联酶标法,检测50例急、慢性病毒性肝炎患者在不同病期时,其外周血T淋巴细胞亚群的变化,结果如下。 材料和方法 一、病例:急性黄疸型肝炎30例,其中甲型和乙型肝炎各半。患者男性21例,女性9例,平均年龄28.7±8.8岁,总胆红质(TBil)71.74±41.31μmol/L,谷丙转氨酶(ALT)均在150u以上(正常<40u)。慢性无黄疸型乙型肝炎20例,其中慢性迁延性肝炎12例,慢性活动性肝炎8例,ALT均在150u以上,男16例,女4例,平均年龄30.1±6.4岁。同时检测10例健康人T细胞亚群,以资对比。     

肺癌患者外周血T淋巴细胞亚群变化特点及临床意义

目的:探讨肺癌患者外周血T淋巴细胞变化及其临床意义。方法:采用流式细胞术检测法检测56例肺癌患者(其中20例早中期肺癌、36例晚期肺癌);18例健康人群外周血单个核细胞(Peripheral blood mononuclear cells,PBMC)中总T细胞(CD3+)、Th细胞(CD3+CD4+)、Tc细胞(CD3+CD8+)、NKT细胞(CD3+CD16+CD56+)、NK细胞(CD3-CD16+CD56+)、调节性T细胞(Treg,CD4+CD25+Foxp3+)占CD4+T细胞比例和CD3+γδT细胞比例。结果:56例肺癌患者总T细胞(CD3+)比例明显低于健康组(61.41%±7.88%vs71.63%±5.59%,P0.001),肺癌患者Tc细胞比例明显低于健康组(23.58%±7.18%vs28.44%±5.20%,P0.05),肺癌患者Treg比例明显高于健康组(6.20%±1.63%vs3.65%±2.00%,P0.001);肿瘤组外周血CD3+γδT细胞比例显著低于健康组(3.35%±1.41%vs5.53%±1.87%,P0.01)。但肺癌患者晚期组与肺癌早中期组比较外周血CD3+γδT细胞比例显著增高(3.70%±1.89%vs2.64%±1.41%,P0.05),肺癌患者晚期组与早中期组比较外周血Treg细胞比较显著增高(6.78%±2.64%vs5.06%±1.22%,P0.05)。肺癌患者外周血中NK细胞低于健康组(15.02%±7.61%vs18.74%±6.39%,P0.05),而Th细胞和NKT细胞都有所降低,但差异尚不具统计学意义(P0.05)。结论:肺癌患者总T细胞、Th细胞、Tc细胞和NK细胞都有所降低,Treg细胞有所上升,提示肺癌患者处于免疫抑制状态。Treg细胞和CD3+γδT细胞与肺癌的临床病程具有一定的关联性。     

多发性硬化患者外周血记忆性T细胞亚群的研究

目的：近来研究表明中心记忆性和效应记忆性T细胞构成记忆性T细胞的两个亚群，但在多发性硬化（Multiple sclerosis，MS）中的作用尚不清楚，因此测定了MS患者外周血记忆性T细胞亚群的水平，并进一步探讨了可能导致记忆性T细胞亚群变化的机制。方法：采用流式细胞仪和酶联免疫吸附分析（Enzyme-linked immunosorbent assay，ELISA）分别检测未治疗MS、正常对照组外周血记忆性T细胞亚群的阳性率和血浆IL-15浓度。进一步根据MS临床表现分为复发-缓解型MS（Relapse-remission MS，RRMS）和慢性进展型MS（Chronic progressiveMS，CPMS）两个亚组。结果：与正常对照比较，在CD8^＋T细胞亚群中，MS患者中心记忆性T细胞（Central memory T cell，TCM）、终末效应记忆性T细胞明显增多和减少（P〈0．05和P〈0．01），RRMS患者终末效应记忆性T细胞明显少于正常对照（P〈0．05）；MS患者血浆IL-15水平较正常对照明显升高（P〈0．05）。结论：研究显示了Ms患者中CD8^＋T CM上调，可能反映了在MS早期被诱导产生的一个持续慢性炎性应答，我们推测CD8^＋T CM的异常改变可能在维持MS慢性炎症的过程中起着重要作用，而IL-15则可能参与了促进TCM分化的调节过程。     

子痫前期患者外周血树突状细胞与T细胞亚群的变化

目的 观察子痫前期患者外周血中的树突状细胞亚群与T细胞亚群相关细胞因子的变化.方法 实验组为子痫前期患者32例,对照组为未孕妇女20例,正常妊娠妇女20例.采集研究对象外周血细胞,流式细胞术检测全血细胞中髓系树突状细胞(mDC)和浆细胞样树突状细胞(pDC);分离外周血单个核细胞,经胞内细胞染色检测Th1、Th2、Th17细胞数量及Th1/Th2比值.结果 子痫前期组mDC百分比(0.33±0.12)％和mDC/pDC比值(2.96±1.65)均高于正常妊娠组,二组数据有明显差异(P＜0.05);pDC百分比(0.16±0.13)％较正常妊娠组(0.21 ±0.12)％有所下降,二组差异有统计学意义(P＜0.05).子痫前期组IFN-γ、IL-4和IL-17的百分比分别为(18.67 ±1.96)％、(1.88±0.51)％和(1.36±0.59)％,与正常妊娠组相比均有显著性差异(P＜0.01).子痫前期组mDC/pDC比率和Th1/Th2之间呈显著正相关(r=0.637,P＜0.01);Th17表达率与pDC表达率之间呈负相关(r=-0.670,P＜0.05),与mDC/pDC比率之间呈显著正相关(r=0.772,P＜0.01).结论 子痫前期患者外周血中树突状细胞亚群和Th1、Th2、Th17型细胞因子异常表达,可能是患者发生免疫失衡的重要原因.     

结缔组织疾病患者外周血T细胞亚群测定

<正> 本文采用人T细胞单克隆抗体OKT系列的直接血球测定法,检测了类风湿性关节炎(RA)及全身性红斑狼疮(SLE)患者共45例,以了解该病治疗前后,T细胞亚群的变化。     

慢性乙型肝炎患者外周血T淋巴细胞亚群的变化

目的了解慢性乙型肝炎患者的细胞免疫功能. 方法用免疫花环法测定41例慢性乙肝患者外周血T细胞亚群并分析其变化. 结果 CD3、CD4细胞以及CD4/CD8比值较正常人显著减少(p<0.01),CD8细胞较正常人明显升高(p<0.01). 结论慢性乙肝患者外周血T细胞亚群紊乱,免疫功能低下.     

麻风患者外周血B细胞和T细胞及其亚群的研究

麻风患者外周血Ｂ细胞和Ｔ细胞及其亚群的研究何浩明，田小平，徐凤英，庄惠琴，徐宁江苏省连云港市第一人民医院临床免疫研究室连云港２２２００２兰义和，徐东升江苏省连云港市皮肤病防治研究所有关麻风患者外周血Ｔ细胞亚群的研究国内外已有报道，但直接检测外周血Ｂ细...     

18例慢性肺心病病人外周血T细胞亚群的变化

我们测定了肺心病病人的淋巴细胞亚群变化,以探讨与细胞免疫功能低下之关系。材料与方法一、实验对象对照组20人,均为本院健康献血员,男14,女6人,平均年龄31岁;病人组18人,男8人,女10人,平均年龄58岁,均为本院住院患者。     

发作期哮喘患者外周血T细胞亚群、B细胞和NK细胞的变化及临床意义

目的：探讨发作期哮喘患者外周血T细胞亚群、B细胞和NK细胞变化及临床意义。方法：采用直接免疫荧光法,用流式细胞术检测30例发作期哮喘患者和30例正常人对照的T细胞亚群、B细胞和NK细胞的变化。结果：与正常对照组比较,发作期哮喘患者CD4^＋T细胞、CD19^＋B细胞和CD4^＋／CD8^＋比值显著增高（P〈0．01）,CD8^＋T细胞显著下降（P〈0．01）和CD56^＋CD16^＋NK细胞下降（P〈0．05）。CD3^＋T细胞无明显变化。结论：发作期哮喘患者的免疫功能紊乱在哮喘发病中起着重要作用。     

颈动脉粥样硬化与腔隙性脑梗塞患者血压近日节律性的分析

目的：探讨合并颈动脉粥样硬化（CAS）的原发性高血压（EH）患者血压近日节律的特征,及与腔隙性脑梗死（CLI）的关系。方法：高血压患者114名,以彩色多普勒检测患者的颈动脉内膜情况及动态血压仪监测患者24小时血压变化,分为CAS组与CAN（颈动脉正常）组,以差值百分比法分析24小时血压节律变化情况,并进行统计学分析。结果：在CAS组的EH患者中,夜间收缩压和舒张压下降率明显低于CAN组患者（P〈O．05）,发生血压近日节律紊乱的患者明显多于CAN组（P〈O．05）。结论：CAS的发生与EH患者血压近日节律的紊乱有密切关系,是缺血性脑卒中发生的危险因素。     

类风湿性关节炎患者外周血TH17细胞测定

目的 探讨新的效应T细胞TH17在类风湿性关节炎(RA)患者外周血的分布及意义.方法 选取PHA或PMA+Ion作为刺激剂,建立流式细胞术胞内细胞因子染色的方法,应用该方法检测了35例活动期、30例稳定期RA患者及正常人外周血TH17和TH1细胞百分率.结果 PlVIA+Ion联合刺激的效果优于PHA.RA患者及正常人T细胞经PMA+Ion刺激后,CD3+CD8-T细胞IL-17表达水平较相应未刺激组显著增加(P<0.05).而不论是否加刺激剂,活动期RA患者外周血CD3+CD8-IL-17+细胞明显多于稳定期,二者均多于正常对照组(P<0.05).RA患者外周血TH1细胞呈现与T<,H>17细胞类似的分布特点.结论 活动期RA患者外周血存在TH17细胞的分布异常,T1H17细胞可作为评价RA患者细胞免疫功能状态的新指标.     

NKT cells: T lymphocytes with innate effector functions

Natural killer T (NKT) cells are innate-like T lymphocytes that recognize glycolipid antigens in the context of the MHC class I-related glycoprotein CD1d. Recent studies have identified multiple ways in which NKT cells can become activated during microbial infection. Mechanisms of CD1d-restricted antigen presentation are being unraveled, and a surprising connection has been made to proteins that control lipid metabolism and atherosclerosis. It appears that several microorganisms have developed strategies to interfere with the CD1d antigen-presentation pathway. New studies have also provided important insight into the mechanisms that control effector cell differentiation of NKT cells and have revealed specialized functions of distinct NKT cell subsets. Finally, there is continued enthusiasm for the development of NKT cell-based therapies of human diseases.     

Activation of cytotoxic T cells and effector cells in experimental autoimmune thyroiditis by shared determinants of mouse and human thyroglobulins

Previous studies have shown that T cells from genetically susceptible mice developing experimental autoimmune thyroiditis (EAT) proliferate in response to restimulation with mouse thyroglobulin (MTg) in vitro and differentiate into cells cytotoxic for syngeneic thyroid monolayers. To examine further the effector cells involved in pathogenesis and the determinants on MTg responsible for their activation, spleen cells (SC) and lymph node cells (LNC) from mice immunized with MTg or human (H) Tg, and adjuvant (complete Freund's adjuvant (CFA) or lipopolysaccharide (LPS] were cultured in vitro with MTg or HTg. Control cultures were incubated with concanavalin A (Con A) or purified protein derivative (PPD). The in vitro-activated cells which proliferated in response to MTg, HTg, or Con A adoptively transferred thyroiditis to normal recipients, whereas cells transferred directly without in vitro culture were very ineffective. The capacity to transfer EAT was abrogated by irradiation (1500 R), and SC from CFA-immunized control mice which responded in vitro to PPD stimulation did not transfer thyroiditis. The serum titers of MTg autoantibodies were uniformly low and were not correlated with severity of disease. The localization of EAT-effector (precursor) cells depended upon the site of immunization; they were found in the spleens after inguinal (subcutaneous) or systemic (intravenous) immunizations, but were present in the popliteal lymph nodes after hind footpad injections. Both homologous MTg and heterologous HTg functioned as in vivo sensitizing antigen and in vitro activating antigen for each other; such cultured cells transferred thyroiditis in vivo and became cytotoxic for thyroid monolayers in vitro. These findings show that shared determinants are autoantigenic and thyroiditogenic, and support the hypothesis that EAT-effector cells responsible for initiating thyroid damage include cytotoxic cells.     

Activation or exhaustion of CD8+ T cells in patients with COVID-19

In addition to CD4⁺ T cells and neutralizing antibodies, CD8⁺ T cells contribute to protective immune responses against SARS-CoV-2 in patients with coronavirus disease 2019 (COVID-19), an ongoing pandemic disease. In patients with COVID-19, CD8⁺ T cells exhibiting activated phenotypes are commonly observed, although the absolute number of CD8⁺ T cells is decreased. In addition, several studies have reported an upregulation of inhibitory immune checkpoint receptors, such as PD-1, and the expression of exhaustion-associated gene signatures in CD8⁺ T cells from patients with COVID-19. However, whether CD8⁺ T cells are truly exhausted during COVID-19 has been a controversial issue. In the present review, we summarize the current understanding of CD8⁺ T-cell exhaustion and describe the available knowledge on the phenotypes and functions of CD8⁺ T cells in the context of activation and exhaustion. We also summarize recent reports regarding phenotypical and functional analyses of SARS-CoV-2-specific CD8⁺ T cells and discuss long-term SARS-CoV-2-specific CD8⁺ T-cell memory.Keywords: CD8⁺ T cell, Activation, T-cell exhaustion, SARS-CoV-2, COVID-19Subject terms: Cellular immunity, Infection