慢性非细菌性前列腺炎/慢性骨盆疼痛综合征患者外周血Th1/Th2细胞的检测

目的:探讨慢性非细菌性前列腺炎/慢性骨盆疼痛综合征(CAP/CPPS)患者外周血Th1/Th2细胞分布的变化情况及其在CAP/CPPS临床分型中的意义。方法:采用流式细胞术检测35例CAP/CPPS患者和12例健康体检者外周血CD3+CD8-T细胞胞内细胞因子干扰素γ(IFN-γ)和白细胞介素4(IL-4)的表达。结果:与正常对照组相比,ⅢA型、ⅢB型CAP/CPPS患者的Th1细胞数均升高,Th1/Th2比值升高,差异有显著性(P<0.05),Th2细胞数差异无统计学意义(P>0.05);ⅢA型与ⅢB型患者比较,Th1、Th2细胞数与Th1/Th2比值差异均无统计学意义(P>0.05)。结论:CAP/CPPS患者Th1型反应模式占优势状态,Th1/Th2平衡失调,Th1/Th2平衡向Th1方向变化,提示Th1细胞在CAP/CPPS的病理发生中可能起重要作用。     

慢性非细菌性前列腺炎/慢性盆腔疼痛综合征与细胞因子的研究现状

慢性前列腺炎(chronic prostatitis,CP)的发病机制复杂,美国国立卫生研究院(NIH)的前列腺炎分类方法中Ⅱ型(慢性细菌性前列腺炎)的发病机制相对明确.Ⅲ型慢性非细菌性前列腺炎/慢性盆底疼痛综合征(CAP/CPPS),即ⅢA、ⅢB,其临床表现为:盆底、会阴部、腰骶部疼痛不适,排尿刺激症状,性功能障碍以及失眠、焦虑等自主神经功能紊乱等,约占临床前列腺病例的90%～95%[1].尽管它不会对患者生命构成威胁,但严重影响患者的生活质量[2],其病因和发病机制尚不明确,在临床工作中诊断和治疗非常棘手.近年来随着分子生物学及免疫学的发展,对于感染性和炎症性疾病发病机制的研究从研究疾病过程中细胞功能转向研究炎症反应应答的调节机制方面.     

吲哚美辛治疗慢性非细菌性前列腺炎/骨盆疼痛综合征患者疼痛的研究

我们采用吲哚美辛治疗以疼痛为主诉的慢性非细菌性前列腺炎 /骨盆疼痛综合征 (CPPS)患者 ,效果较好 ,现报告如下。材料与方法　本组 180例。年龄18～ 4 9岁 ,平均 31岁。病史 3个月～ 4年。患者均以下腹部、会阴区、腰骶部、睾丸阴囊疼痛为主诉 ,分别伴有性功能减退、尿频等症状。均根据病史、症状和Meares Stamey“四杯法”诊断为CPPS ,并系统检查除外其他可能引起上述疼痛的疾病。 180例随机分为吲哚美辛组、左氧氟沙星组、特拉唑嗪组 3组 ,每组6 0例。吲哚美辛组肛塞吲哚美辛 10 0mg ,根据疼痛程度 1～ 2次 /d。左氧氟沙星组口服左氧…     

慢性非细菌性前列腺炎/慢性盆底疼痛综合征患者症状与白细胞计数的关系

目的探讨慢性非细菌性前列腺炎/慢性盆底疼痛综合征患者(CAP/CPPS)症状与前列腺液、按摩后尿液、精液中白细胞计数间的关系.方法以前列腺炎症状评分(NIH-CPS1)评估CAP/CPPS患者症状情况,按四杯法留取尿液,对患者前列腺液、按摩后尿液、精液行白细胞计数,并对样本行细菌培养.将228例CAP/CPPS患者分型,对患者症状与实验室结果间行相关分析.结果CAP/CPPS患者中,依据EPS、VB3或精液中WBC数目而分型的Ⅲ a型与Ⅲ b患者间的CPSI中的疼痛、排尿不适、生活质量及总分无显著性差异(P值分别为0.97、0.75、0.08、0.55).CAP/CPPS患者EPS、VB3或精液中WBC数目与CPSI中的疼痛、排尿不适、生活质量及总分无显著相关性(P值＞0.05).结论CAP/CPPS患者Ⅲ a型与Ⅲ b型间症状严重程度无显著性差异,白细胞计数与CAP/CPPS患者症状的严重程度无明显相关性,提示还有其他引起CPPS症状的因素存在.     

慢性非细菌性前列腺炎/慢性盆腔疼痛综合征患者前列腺液中炎症因子差异表达的临床意义

目的 探讨慢性非细菌性前列腺炎/慢性盆腔疼痛综合征(CAP/CPPS)患者前列腺液(EPS)中炎症因子差异表达的临床意义.方法选取符合CAP/CPPS诊断标准的患者EPS标本38例(CAP 18例,CPPS 20例),20例健康者EPS标本作对照.应用抗体芯片检测EPS中40种炎症因子的表达差异.结果 与对照组比较,CAP患者7种炎症因子包括单核细胞趋化因子(MCP)-1、可溶性肿瘤坏死因子受体Ⅱ(s TNF RⅡ)、血小板衍生生长因子-BB(PDGF-BB)、白细胞介素(IL)-1β、IL-11、IL-6、MCP-2表达增高了1.50倍以上,CPPS患者5种炎症因子包括MCP-1、PDGF-BB、MCP-2、s TNF RⅡ、IL-11表达增高了1.50倍以上;聚类分析结果表明,MCP-1、PDGF-BB为最后聚合的炎症因子,CAP组中分别上调3.47、2.07倍,CPPS组中分别上调2.25、2.19倍;与CPPS组比较,CAP组IL-1β,MCP-1、S TNF RⅡ表达分别上调1.85、1.55、1.67倍.结论 CAP/CPPS发病过程中炎症因子表达明显增高,CAP的炎症反应程度高于CPPS,MCP-1、PIX;F-BB有可能成为CAP/CPPS诊断的炎症标志物.     

慢性非细菌性前列腺炎/慢性盆腔疼痛综合征患者前列腺液中炎症因子差异表达的临床意义

Objective To investigate the role of inflammatory cytokines in the pathogenesis of chronic non-bacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS) patients. Methods The 38 cases with CAP/CPPS patients (18 cases of CAP and 20 cases of CPPS) and 20 cases of healthy controls were selected. The differential expressions of 40 kinds of inflammatory cytokines were detec-ted by antibody arrays in prostate fluid. Results The inflammatory cytokines which increased more than 1.5 times expression have been found. There were seven kinds in CAP including monocyte che-moattractant protein (MCP)-1, solution tumor necrosis factor receptor Ⅱ(s TNF R Ⅱ), platelet-de-rived growth faetor-BB (PDGF-BB), interleukin (IL)-β, IL-11、IL-6、MCP-2 and five kinds in CPPS groups including MCP-1、PDGF-BB、MCP-2、s TNF R Ⅱ、It-11 respectively, compared with healthy control group. The cluster analysis results showed that protein expression of Monocyte chemoattrac-tant protein 1 (MCP-1)and platelet-derived growth factor BB (PDGF-BB) were significantly increased in CAP (3.47 and 2.07 times) and CPPS (2.25 and 2.19 times) compared with healthy control group and were the final polymerization of inflammatory cytokines. The protein expression of interleukin 1 β (IL-1 β), MCP-1 and soluble tumor necrosis factor Ⅱ (s TNF R Ⅱ) in CAP group was increased more than 1.85,1.55,1.67 times compared with CPPS group. Conclusions Elevated expression of inflammatory cytokines may play an important role in the course of CAP/CPPS disease. The extent of the inflammatory response of CAP was higher than CPPS. The inflammatory factors of MCP-1 and PDGF-BB could serve as a novel diagnostic marker.     

慢性非细菌性前列腺炎/慢性盆腔疼痛综合征患者前列腺液中炎症因子差异表达的临床意义

Objective To investigate the role of inflammatory cytokines in the pathogenesis of chronic non-bacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS) patients. Methods The 38 cases with CAP/CPPS patients (18 cases of CAP and 20 cases of CPPS) and 20 cases of healthy controls were selected. The differential expressions of 40 kinds of inflammatory cytokines were detec-ted by antibody arrays in prostate fluid. Results The inflammatory cytokines which increased more than 1.5 times expression have been found. There were seven kinds in CAP including monocyte che-moattractant protein (MCP)-1, solution tumor necrosis factor receptor Ⅱ(s TNF R Ⅱ), platelet-de-rived growth faetor-BB (PDGF-BB), interleukin (IL)-β, IL-11、IL-6、MCP-2 and five kinds in CPPS groups including MCP-1、PDGF-BB、MCP-2、s TNF R Ⅱ、It-11 respectively, compared with healthy control group. The cluster analysis results showed that protein expression of Monocyte chemoattrac-tant protein 1 (MCP-1)and platelet-derived growth factor BB (PDGF-BB) were significantly increased in CAP (3.47 and 2.07 times) and CPPS (2.25 and 2.19 times) compared with healthy control group and were the final polymerization of inflammatory cytokines. The protein expression of interleukin 1 β (IL-1 β), MCP-1 and soluble tumor necrosis factor Ⅱ (s TNF R Ⅱ) in CAP group was increased more than 1.85,1.55,1.67 times compared with CPPS group. Conclusions Elevated expression of inflammatory cytokines may play an important role in the course of CAP/CPPS disease. The extent of the inflammatory response of CAP was higher than CPPS. The inflammatory factors of MCP-1 and PDGF-BB could serve as a novel diagnostic marker.     

慢性非细菌性前列腺炎/慢性盆腔疼痛综合征患者前列腺液中炎症因子差异表达的临床意义

Objective To investigate the role of inflammatory cytokines in the pathogenesis of chronic non-bacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS) patients. Methods The 38 cases with CAP/CPPS patients (18 cases of CAP and 20 cases of CPPS) and 20 cases of healthy controls were selected. The differential expressions of 40 kinds of inflammatory cytokines were detec-ted by antibody arrays in prostate fluid. Results The inflammatory cytokines which increased more than 1.5 times expression have been found. There were seven kinds in CAP including monocyte che-moattractant protein (MCP)-1, solution tumor necrosis factor receptor Ⅱ(s TNF R Ⅱ), platelet-de-rived growth faetor-BB (PDGF-BB), interleukin (IL)-β, IL-11、IL-6、MCP-2 and five kinds in CPPS groups including MCP-1、PDGF-BB、MCP-2、s TNF R Ⅱ、It-11 respectively, compared with healthy control group. The cluster analysis results showed that protein expression of Monocyte chemoattrac-tant protein 1 (MCP-1)and platelet-derived growth factor BB (PDGF-BB) were significantly increased in CAP (3.47 and 2.07 times) and CPPS (2.25 and 2.19 times) compared with healthy control group and were the final polymerization of inflammatory cytokines. The protein expression of interleukin 1 β (IL-1 β), MCP-1 and soluble tumor necrosis factor Ⅱ (s TNF R Ⅱ) in CAP group was increased more than 1.85,1.55,1.67 times compared with CPPS group. Conclusions Elevated expression of inflammatory cytokines may play an important role in the course of CAP/CPPS disease. The extent of the inflammatory response of CAP was higher than CPPS. The inflammatory factors of MCP-1 and PDGF-BB could serve as a novel diagnostic marker.     

慢性非细菌性前列腺炎/慢性盆腔疼痛综合征患者前列腺液中炎症因子差异表达的临床意义

Objective To investigate the role of inflammatory cytokines in the pathogenesis of chronic non-bacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS) patients. Methods The 38 cases with CAP/CPPS patients (18 cases of CAP and 20 cases of CPPS) and 20 cases of healthy controls were selected. The differential expressions of 40 kinds of inflammatory cytokines were detec-ted by antibody arrays in prostate fluid. Results The inflammatory cytokines which increased more than 1.5 times expression have been found. There were seven kinds in CAP including monocyte che-moattractant protein (MCP)-1, solution tumor necrosis factor receptor Ⅱ(s TNF R Ⅱ), platelet-de-rived growth faetor-BB (PDGF-BB), interleukin (IL)-β, IL-11、IL-6、MCP-2 and five kinds in CPPS groups including MCP-1、PDGF-BB、MCP-2、s TNF R Ⅱ、It-11 respectively, compared with healthy control group. The cluster analysis results showed that protein expression of Monocyte chemoattrac-tant protein 1 (MCP-1)and platelet-derived growth factor BB (PDGF-BB) were significantly increased in CAP (3.47 and 2.07 times) and CPPS (2.25 and 2.19 times) compared with healthy control group and were the final polymerization of inflammatory cytokines. The protein expression of interleukin 1 β (IL-1 β), MCP-1 and soluble tumor necrosis factor Ⅱ (s TNF R Ⅱ) in CAP group was increased more than 1.85,1.55,1.67 times compared with CPPS group. Conclusions Elevated expression of inflammatory cytokines may play an important role in the course of CAP/CPPS disease. The extent of the inflammatory response of CAP was higher than CPPS. The inflammatory factors of MCP-1 and PDGF-BB could serve as a novel diagnostic marker.     

慢性非细菌性前列腺炎/慢性盆腔疼痛综合征患者前列腺液中炎症因子差异表达的临床意义

Objective To investigate the role of inflammatory cytokines in the pathogenesis of chronic non-bacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS) patients. Methods The 38 cases with CAP/CPPS patients (18 cases of CAP and 20 cases of CPPS) and 20 cases of healthy controls were selected. The differential expressions of 40 kinds of inflammatory cytokines were detec-ted by antibody arrays in prostate fluid. Results The inflammatory cytokines which increased more than 1.5 times expression have been found. There were seven kinds in CAP including monocyte che-moattractant protein (MCP)-1, solution tumor necrosis factor receptor Ⅱ(s TNF R Ⅱ), platelet-de-rived growth faetor-BB (PDGF-BB), interleukin (IL)-β, IL-11、IL-6、MCP-2 and five kinds in CPPS groups including MCP-1、PDGF-BB、MCP-2、s TNF R Ⅱ、It-11 respectively, compared with healthy control group. The cluster analysis results showed that protein expression of Monocyte chemoattrac-tant protein 1 (MCP-1)and platelet-derived growth factor BB (PDGF-BB) were significantly increased in CAP (3.47 and 2.07 times) and CPPS (2.25 and 2.19 times) compared with healthy control group and were the final polymerization of inflammatory cytokines. The protein expression of interleukin 1 β (IL-1 β), MCP-1 and soluble tumor necrosis factor Ⅱ (s TNF R Ⅱ) in CAP group was increased more than 1.85,1.55,1.67 times compared with CPPS group. Conclusions Elevated expression of inflammatory cytokines may play an important role in the course of CAP/CPPS disease. The extent of the inflammatory response of CAP was higher than CPPS. The inflammatory factors of MCP-1 and PDGF-BB could serve as a novel diagnostic marker.     

调节性T细胞及其细胞因子在慢性无菌性前列腺炎的表达及意义

目的 观察调节性T细胞(Tr)在慢性无菌性前列腺炎(CAP)发病机制的作用及意义.方法 使用流式细胞术检测20例CAP患者及10例健康志愿者外周血Tr的数量;用RTPCR法检测Tr的调节蛋白Foxp3mRNA的表达含量;用ELISA法两组前列腺按摩液细胞因子白介素-10(IL-10)及转化生长因子-β1(TGF-B1)...     

CD4＋CD25＋调节性T细胞与Foxp3表达在白癜风发病中的作用

目的：研究CD4＋CD25＋调节性T细胞（CD4＋CD25＋Treg细胞）与Foxp3基因表达与白癜风发病的关系及可能机制。方法：以确诊为进展期白癜风且治疗显效的24例患者为研究对象,患者确诊符合白癜风诊断及疗效标准。以16例健康志愿者作为对照。应用流式细胞术检测正常对照、白癜风患者治疗前后各自外周血中CD4＋CD25＋调节性T细胞的比例。采用密度梯度离心法从治疗前后的外周血中提取单个核细胞,以逆转录聚合酶链扩增方法检测其中Foxp3 mRNA的表达水平。结果：进展期且治疗显效的24例白癜风患者外周血中CD4＋CD25＋调节性T细胞的比例以及CD4＋CD25＋调节性T细胞在总CD4＋T细胞中所占比例明显均低于正常对照组（P〈0．05）。治疗后显效的进展期白癜风患者CD4＋CD25＋调节性T细胞的比例与治疗前相比明显升高（P〈0．05）,CD4＋CD25＋调节性T细胞中Foxp3 mRNA的表达水平比治疗也前明显增加（P〈0．05）。结论：进展期白癜风患者体内存在CD4＋CD25＋调节性T细胞的异常,CD4＋CD25＋Treg细胞的数量的减少和Foxp3表达的降低所造成的CD4＋CD25＋Treg细胞免疫抑制功能爱损可能是白癜风发病的一个因素。     

CD4+CD25+ regulatory T cells mediate acquired transplant tolerance

The Holy Grail of clinical organ transplantation is the safe induction of allograft tolerance. Transplant tolerance has been successfully induced in animal models. Since T cells play a pivotal role in graft rejection, modulating T cell function has been the primary focus of studies aimed at inducing transplant tolerance. Rodent models of transplant tolerance induction include central deletion and peripheral mechanisms involving activation-induced cell death (AICD), anergy, immune deviation, and production of regulatory T cells. These mechanisms are not mutually exclusive. Although clonal deletion and anergy limit self-reactive T cells in the thymus, these mechanisms alone are not sufficient for controlling self-reactive T cells in the periphery. There is now evidence that the adult animal harbors two functionally distinct populations of CD4(+) T cells; one mediates autoimmune disease and the other dominantly inhibits it. The latter cells express CD4, CD25 and CTLA-4. These thymus-derived T cells have recently been shown to mediate the induction and maintenance of transplant tolerance. These CD4(+)CD25(+) T cells are similar in origin, phenotype, and function to those that maintain natural self-tolerance and T cell homeostasis in the periphery. Against this background, is it possible that alloantigen specific regulatory T cells might be generated and expanded ex vivo before organ transplantation and then infused to induce long-term tolerance, perhaps without the need for chronic immunosuppression?     

CD4+CD25+调节性T细胞/辅助性T细胞17在脓毒症大鼠中的作用

目的 观察CD4+ CD25+调节T细胞(Treg)/辅助性T细胞17(Th17)细胞在脓毒症大鼠炎性免疫反应中的作用.方法 110只雄性SD大鼠随机分为正常对照组、假手术组、脓毒症(CLP)组,采用改良的盲肠结扎穿孔术(CLP)制作大鼠脓毒症模型.采用流式细胞术检测CD14+单核细胞表面人类白细胞抗原-DR基因(HLA-DR)表达率、Treg细胞及TH17细胞比例;酶联免疫吸附试验(ELISA)检测白细胞介素(IL)-6、IL-10、肿瘤坏死因子(TNF)-α、转化生长因子(TGF)-β、白细胞介素(IL)-17炎性因子蛋白表达.结果 与假手术组比较:(1)伴随着脓毒症病情的发展,大鼠出现明显的免疫抑制,CD14+单核细胞HLA-DR表达率＜30％,IL-10/TNF-α比值(27.41 ±7.04比6.63 ±2.60)明显增高(P＜0.01).(2)术后96 h脓毒症大鼠Treg细胞[(11.91±3.88)％比(6.57±2.60)％,P＜0.01]和Th17细胞[(5.14±0.29)％比(2.85±0.07)％,P＜0.01]表达明显增高.(3)术后96 h脓毒症组前炎性细胞因子IL-6[(42.31±15.89) ng/L比(6.32 ±3.18) ng/L,P＜0.01]、IL-10[(69.89 ±20.78) ng/L比(13.58±5.37) ng/L,P＜0.01]、TNF-α[(5.03±3.10) ng/L比(2.77±1.10) ng/L,P＜0.01]、TGF-β[(4.99±2.01) ng/L比(1.88±1.07) ng/L,P＜0.01]、IL-17[(92.77±11.64) ng/L比(7.58±2.30) ng/L,P＜0.01]表达明显增高.结论 伴随着脓毒症病情的发展,大鼠出现明显的免疫抑制;在大鼠脓毒症的发生发展中,Treg细胞介导的免疫抑制及Th17细胞介导免疫激活反应同时存在;脓毒症细胞因子微环境变化可能是导致Treg细胞/Th17细胞失衡的原因之一.     

大鼠CD4^＋CD25^＋调节性T细胞的分离及功能鉴定

目的：研究利用免疫磁珠分选法稳定分离正常大鼠脾脏CD4^＋CD25^＋调节性T细胞的方法。方法：采用免疫磁珠两步法分离大鼠脾组织CD4^＋CD25^＋T细胞。首先采用藻红蛋白（PE）标记的抗CD25抗体和抗PE多功能磁珠试剂盒阳性分选CD25^＋T细胞,再用抗异硫氰酸荧光素（FITC）标记抗体和抗IgG磁珠阳性分选获得CD4^＋CD25^＋T细胞。分离后的细胞经流式细胞仪检测分离纯度,台盼蓝染色检测细胞存活率,体外增殖实验检测其对CD4^＋CD25^-T细胞的免疫抑制作用。结果：两次阳性分选后获得的CD4^＋CD25^＋T细胞纯度为（90.4±1.6）%,细胞存活率为（92.6±2.4）%。体外增殖实验表明,CD4^＋CD25^＋T细胞能明显抑制CD4^＋CD25^-T细胞的增殖（P〈0.01）。结论：采用免疫磁珠法两次阳性分选,可稳定地获得纯度理想并有免疫抑制功能的大鼠CD4^＋CD25^＋T细胞。     

慢性乙型肝炎患者外周血调节性T细胞对树突状细胞功能的抑制作用

目的研究慢性乙型肝炎（CHB）患者外周血CD4＋CD25＋调节性T细胞（Treg）对树突状细胞（DCs）免疫功能的抑制作用,探讨治疗CHB的新方法。方法采用密度梯度离心法获得CHB患者和健康对照组（NC组）外周血单个核细胞（PBMC）;部分PBMC体外诱导培养获得DCs,部分PBMCs用特异性免疫磁珠分选获得CD4＋CD25＋Treg和CD4＋CD25-T细胞;不同来源的DCs和正常对照组CD4＋CD25-T细胞混合为反应细胞,将不同来源和不同比例的Treg分别加入到反应细胞中培养3 d,MTT法检测Treg抑制DCs的抑制指数（SI）,并在培养DCs的不同时间加入Treg,应用流式细胞术检测DCs表面共刺激分子CD80和HLA-DR的表达。结果来源于CHB患者及NC组的Treg均可抑制DCs的免疫作用,来源于CHB患者Treg抑制DCs能力显著高于NC,差异具有统计学意义（P ＜0.01）。不同比例的Treg均可抑制DCs的免疫功能,随着Treg比例的增高抑制作用也越明显,抑制指数亦越高。在DCs培养的不同时间加入相同比例的Treg,发现Treg对DCs表面分子CD80、HLA-DR的表达均有抑制作用,与对照组相比,差异具有统计学意义（P＜0.01）,同时发现加入Treg的时间越早,DCs表面分子表达降低越明显。结论 CHB患者Treg可显著抑制DCs免疫功能且呈时间和量的依赖,抑制DCs表面分子CD80和HLA-DR表达,可能是Treg抑制DC免疫功能的机制之一。     

胃癌患者外周血调节性T细胞的多种细胞因子水平的检测及其意义

目的探讨细胞因子在CD4^＋CD25^＋调节性T细胞免疫抑制机制中的作用，观察胃癌患者外周血中的CD4^＋CD25^＋调节性T细胞及其效应性T细胞CD4^＋CD25^-T细胞产生具有不同生物活性的细胞因子的水平。方法采用免疫磁珠分选方法分离胃癌患者外周血中的CD4^＋CD25^＋T细胞与CD4^＋CD25^-T细胞后，将CD4^＋CD25^＋T细胞与效应性T细胞CD4^＋CD25^-T细胞在体外分别单独培养及按不同比例共同培养后，再用酶联免疫吸附试验（ELISA）法检测单独及混合培养时细胞因子干扰素（IFN）-γ、白细胞介素（IL）-10及转化生长因子（TGF）-β分泌的水平。结果健康对照及胃癌患者CD4^＋CD25^＋T细胞分泌抑制性细胞因子IL-10、TGF-β均显著高于CD4^＋CD25^-T细胞，而分泌细胞因子IFN-γ均显著低于CD4^＋CD25^-T细胞（P〈0．01）。CD4^＋CD25^＋T细胞在体外可明显抑制CD4^＋CD25^-T细胞产生IFN-γ的能力，且这种抑制能力呈效靶比关系（P〈0．01）；但CD4^＋CD25^＋T细胞与效应性T细胞CD4^＋CD25^-T细胞在体外共培养对IL-10及TGF-β的分泌无显著影响（P〉0．01）。结论CD4^＋CD25^＋调节性T在体外可能通过细胞因子的调节发挥对效应性T细胞的抑制作用。     

调节性CD4~+CD25~+T细胞的分离纯化及免疫功能研究

目的 制备调节性CD~+ CD25~+T细胞(Treg)分析其免疫功能,诱导局部免疫耐受防治同种异体复合组织移植(CTA)排斥反应.方法 采用免疫磁珠法(MACS)从雄性大鼠脾脏细胞分离CD4~+CD25~+Treg(1×10~6),2%锥虫蓝染色检测活性、流式细胞术分析其纯度,在5 mg/L抗CD3的刺激下观察其反应性、增殖及其与200 U/ml细胞介素(IL)-2的关系.结果 从8只雄性大鼠脾脏分选出的CD4~+CD25~+Treg活性平均为(97.90±0.36)%及纯度为(96.05±0.41)%,CD3刺激呈低反应,按比例培养抑制率为89%,IL-2可使CD4~+CD25~-抑制逆转.结论 MACS能快速分选出较高纯度的CD4~+CD25~+Treg,并且活性良好在体外具有免疫无能及免疫抑制作用,能满足动物CTA排斥反应研究的需要.     

重症急性胰腺炎患者外周血CD4+CD25high调节性T细胞的动态变化研究

目的 动态观察重症急性胰腺炎(severe acute pancreatitis,SAP)患者外周血CD4+CD25 high调节性T细胞(Treg)和Foxp3及细胞因子IL-10、IFN-γ及IL-4的变化,探讨其临床意义.方法 将2008年8月-2009年6月收治的42例SAP患者根据病程的变化分为3期:Ⅰ期(全身炎症反应综合征期即SIRS期);Ⅱ期(SIRS下调期);Ⅲ期(感染相关并发症期).对照组为同期住院的38例急性轻型胰腺炎(MAP)患者.分别抽取外周血,以流式细胞仪检测Treg及Foxp3百分率,酶联免疫吸附法(ELISA)检测IFN-γ、IL-4及IL-10的水平,并对以上指标进行相关性分析.结果 Treg百分率和IL-4水平在SAP Ⅰ期开始升高(Treg:1.37%±1.12%;IL-4:22.92±4.17),Ⅱ期高于Ⅰ期(Treg:3.12%±1.21%;IL-4:35.42±12.50),Ⅲ期升至最高(Treg:4.47%±1.04%;IL-4:76.04±14.58);IFN-γ水平在SAP Ⅰ期最高(978.57±213.29),Ⅱ期降低(571.43±157.14),在Ⅲ期降至最低(357.14±150.00);各期相比差异有统计学意义(P＜0.05),且均明显高于对照组(P＜0.05).Treg比例与IFN-γ水平负相关(r=-0.895,P＜0.01),与IL-4水平正相关(r=0.813,P＜0.01).结论 Treg可能通过抑制IFN-γ的分泌及促进IL-4的产生,对抗过度炎症反应对机体造成的损害.