特发性血小板减少性紫癜患者外周血淋巴细胞协同刺激分子B7的表达

目的　探讨B淋巴细胞表面协同刺激分子B7(B7 1、B7 2 )在特发性血小板减少性紫癜 (ITP)中的变化。方法　用流式细胞术检测 30例初发ITP患者和 15例正常人对照外周血淋巴细胞协同刺激分子B7 1(CD80 + )、B7 2 (CD86 + )表达率。结果　ITP患者外周血淋巴细胞CD86 + 、B细胞表面CD86 (CD1 9+ CD86 + CD1 9+ )表达率明显高于正常人 (P <0 .0 5 ) ,而CD80 + 、CD1 9+ CD80 + CD1 9+ 表达率相对于正常人无显著性差异 (P >0 .0 5 )。结论　ITP患者CD86 + 的改变可能参与ITP自身免疫的病理机制     

特发性血小板减少性紫癜患者外周血淋巴细胞亚群和血小板相关抗体变化及临床意义

用流式细胞术直接免疫法检测l72例早期特发性血小板减少性紫癜(ITP)患者外周血淋巴细胞亚群(CD3、CD4、CD8、CD19、C16、CD56)，ELISA法检测血小板表面血小板相关抗体(PAIgG、PAIgA、PAIgM)。结果显示，ITP组与正常对照组比较CD3、CD4／CD8显著降低(P＜0.01)，CD8增高(P＜0．05)，CD19增高极为显著(P＜0．01)；ITP血小板表面PAIgG、PAIgA、PAIgM显著高于对照组；CD19升高和CD4/CD8下降与PAIgG、PAIgA、PAIgM增高有显著的相关性。认为淋巴细胞亚群功能和比例失常、T细胞免疫调节机制紊乱在ITP的发病机制中起非常重要的作用。     

特发性血小板减少性紫癜患者血小板抗体等四项参数测定的价值

目的　探讨特发性血小板减少性紫癜 (ITP)患者血小板抗体 (PAIgG)、血小板膜蛋白(CD62P)、网织血小板 (RP)及淋巴细胞亚群变化及意义。方法　应用流式细胞术检测 5 8例ITP组及 2 0例正常对照组外周PAIgG、血CD62P、RP、淋巴细胞亚群的表达。结果　ITP组的血小板数明显低于正常对照组 (P <0 .0 1) ,PAIgG、CD62P、RP均明显高于正常对照组 (P <0 .0 1)。在淋巴细胞亚群中 ,ITP组CD3、CD4、CD4/CD8比值明显低于正常对照组 (P <0 .0 1) ,CD8、CD19细胞则显著高于正常对照组 ,而CD16+ 5 6与正常对照组无明显差异。结论　PAIgG、CD62P、RP及淋巴细胞亚群的变化可较好地反映ITP这一病理过程 ,对提高诊断水平及指导临床有一定实用价值。     

强直性脊柱炎患者外周血CD28 CD40共刺激通路相关分子的表达

目的探讨强直性脊柱炎(AS)患者外周血淋巴细胞CD28和CD40共刺激通路相关分子的表达及其与免疫功能紊乱的关系。方法采用流式细胞仪检测69例AS初诊患者和50名健康对照者CD28、CTLA-4和CD40L在外周血CD3~ T细胞上的表达及CD80、CD86和CD40在CD19~ B细胞上的表达。用ELISA法测定血清中免疫球蛋白IgG、IgA和IgM的水平。结果AS患者CD3~ T细胞上的CD28、CTLA-4和CD40L,CD19~ B细胞上CD86和CD40的表达均较正常对照组显著增高(P＜0．01),CD80在CD19 B细胞表达增高(P＜0．05)：AS患者血清中2种免疫球蛋白IgG、IgA的水平较正常对照组显著增高(P＜0．01)。结论AS患者CD28和CD40共刺激通路相关分子表达增强,机体处于免疫激活状态,CD28和CD40共刺激通路在AS的发病中可能起重要作用。     

ITP患者外周血淋巴细胞共刺激分子表达及意义

目的　研究共刺激分子在特发性血小板减少性紫癜 (ITP)外周血淋巴细胞的表达 ,并探讨其发病机制。方法　应用流式细胞术检测 2 8例 ITP患者及 15例正常对照者的外周血淋巴细胞 CD80 、CD2 8、CD86 表达 ,用酶联免疫吸附法检测血小板相关抗体 (PAIg G)水平 ;并与患者的临床资料进行相关性分析。结果　 1ITP组外周血淋巴细胞 CD2 8表达率降低 ,CD80 表达率略增加 ,与对照组均无统计学差异 ;CD86 表达率明显高于对照组 (P<0 .0 1)。 2 ITP组 2 1例 PAIg G水平升高 ,均值为 (197.39± 6 7.81) ng/ 10 7PA。 3ITP组外周血淋巴细胞 CD86 表达率与其巨核细胞数值呈正相关 (P<0 .0 5 )。结论　 ITP患者外周血淋巴细胞共刺激分子 CD2 8、CD80 表达无缺陷 ;CD86 表达明显增加。表明 CD86 可能参与 ITP的发病机制 ,应用抗 CD86 单克隆抗体方法可能治疗 ITP。     

共刺激分子CD28 CD152在类风湿关节炎患者T细胞亚群上表达异常的研究

目的观察共刺激分子CD28,CD152在类风湿关节炎(RA)患者的T细胞亚群上的表达异常情况,探讨RA的发病机制及治疗手段.方法用流式细胞仪采用直接免疫荧光法测定39例RA患者和20名健康对照人外周血T细胞表面标志CD3,CD4,CD8的表达情况及CD28,CD152在CD4+T和CD8+T细胞上的表达.结果 RA患者CD3+CD4+细胞较正常对照组显著增高(P＜0.01),CD3+CD8+细胞较正常对照组显著降低(P＜0.05),CD4+T细胞上CD28的表达较对照组显著降低(P＜0.05),而CD8+T细胞上CD28的表达与对照组差异无显著性(P＞0.05);CD4+T和CD8+T细胞上CD152的表达都较对照组显著增高(P＜0.01).结论在RA患者的细胞免疫活化过程中首先表现为B7/CD28信号途径占优势,T细胞被激活,激活的T细胞大量分泌CD152,它与CD28竞争结合B7分子,CD152/B7途径转而占优势,下调或终止T细胞反应.同时CD28+细胞数目的减少或功能缺陷造成RA患者外周血单个核细胞凋亡加速,是诱发RA患者的局部病理损害的原因.阻断CD152和B7的相互作用可增强特异性T细胞应答,为RA的免疫学治疗提供理论依据.     

细胞免疫及体液免疫在ITP发生发展中的作用及其机制探讨

目的用ELISA法检测60例特发性血小板减少性紫癜(ITP)患者(观察组)血小板相关抗体PAIgG、PAIgA、PAIgM,免疫比浊法(ITM)测定补体C3、C4,流式细胞仪直接免疫法检测外周血淋巴细胞亚群(CD3、CD4、CD8、CD 16 CD56)水平,并与30例健康人(对照组)比较。结果与对照组比较,观察组血小板相关抗体PAIgG、PAIgA、PAIgM均显著升高,补体C3显著降低,C4无明显变化;外周血淋巴细胞亚群CD3显著降低,CD8增高,CD4/CD8下降,CD16 CD56降低。证实T细胞免疫调节机制紊乱、淋巴细胞功能和比例失调在ITP的发生中起非常重要的作用。     

类风湿关节炎患者外周血CD19+CD23+B淋巴细胞水平及其与疾病活动性的关系

目的 探讨类风湿关节炎(RA)患者外周血CD19+ CD23+B淋巴细胞检测水平与病情活动性的相关性.方法 选择RA患者50例(RA组)及健康体检者20例(对照组),分别采用流式细胞仪检测两组外周血CD19+ CD23+B淋巴细胞水平,分析其与RA患者疾病活动度的相关性.结果 RA组患者外周血CD19+、CD23+及CD23 +/CD19+细胞百分率均明显较正常对照组升高(P＜0.05).CD19+表达率与晨僵时间、关节压痛数、关节肿胀数、RF、PLT、DAS28呈正相关(均P＜0.05),而与ESR、C-反应蛋白无明显相关(均P＞0.05).CD23+及CD23 +/CD19+表达率与晨僵时间、关节压痛数、关节肿胀数、ESR、CRP、RF、PLT、DAS28呈显著正相关关系(均P＜0.05).结论 外周血中CD19+、CD23+及CD23+/CD19+淋巴细胞的异常表达在RA发病机制中可能起一定作用,且与疾病活动性相关.     

特发性血小板减少性紫癜患者免疫相关指标的检测及其临床意义

目的 检测特发性血小板减少性紫癜(ITP)患者免疫相关指标的变化,探讨其在ITP发病机制中的作用及其临床意义.方法 应用酶联免疫斑点技术(ELISPOT)、改良血小板抗原单克隆抗体固相化检测技术(MAIPA)、流式细胞术及夹心法ELISA分别检测64例1TP患者及31例正常对照者分泌GPⅡb/Ⅲa抗体B细胞、血小板特异性抗体(抗GPⅡb/Ⅲa抗体、抗GP I b/Ⅸ抗体)、T淋巴细胞亚群、网织血小板(RP)及血小板生成素(TPO)的变化.结果 ITP患者分泌GPⅡb/Ⅲa抗体B细胞频数[急性ITP组患者为7.6±4.6/105个外周血单个核细胞(PBMC),慢性ITP组患者为5.3±3.0/105个PBMC]、血小板特异性抗体(抗GPⅡb/Ⅲa抗体、抗GPI b/Ⅸ抗体)的吸光度值(急性ITP组患者为0.51±0.11、0.48±0.06,慢性ITP组患者为0.49±0.10、0.46±0.09)、CD8+T淋巴细胞百分比[(27.09±9.86)%]、RP百分比[巨核细胞增多组为(24.85±19.18)%,巨核细胞正常组为(23.89±18.90)%]明显高于正常对照组[1.3±0.5/105个PBMC,0.33±0.06,0.41±0.03,(22.08±4 54)%,(8.19±2.46)%,P值均＜0.05],其中急性ITP患者分泌GPⅡb/Ⅲa抗体B细胞高于慢性ITP患者(P＜0.05).ITP组CD3+T淋巴细胞百分比、CD4+T淋巴细胞百分比及CD4+/CD8+比值[(60.88±14.59)%、(28.41±10.55)%、1.18±0.59]均低于正常对照组[(69.89±6.43)%、(35.38±5.05)%、1.64±0.29,P值均＜0.05].ITP患者巨核细胞增多组TPO水平(72.09±41.64)明显低于ITP患者巨核细胞正常组(118.60±70.72,P＜0.05),与正常对照组(75.37±26.32)之间差异无统计学意义(P＞0.05).结论 分泌GPⅡb/Ⅲa抗体B细胞、血小板特异性抗体、T淋巴细胞亚群、RP%及TPO在ITP诊断及指导定向干预治疗中有一定的意义.     

初发过敏性紫癜患儿外周血CD4+CD28-和CD8+CD28-T细胞水平变化及意义

目的 观察初发过敏性紫癜(HSP)患儿外周血T淋巴细胞亚群(CD4+ CD28-T细胞和CD8+ CD28-T细胞)的表达变化,并探讨其临床意义.方法 采用流式细胞技术(FCM)检测89例初发HSP患儿(HSP组)和30例健康儿童(对照组)外周血T淋巴细胞免疫表型.结果 HSP组CD4+ CD28+、CD8+ CD28+、CD3+ CD4+T淋巴细胞表达水平及CD4+/CD8+比率较对照组显著降低(P均＜0.05);HSP组CD3+和CD3+ CD8+T淋巴细胞表达水平与对照组相比无显著性差异(P＞0.05);HSP组CD4+ CD28-T细胞和CD8+ CD28-T细胞较对照组明显增高(P均＜0.05),但在皮肤型、关节型、腹型、混合型和紫癜性肾炎五种临床类型间无明显差别(P均＞0.05).结论 HSP患儿存在T淋巴细胞亚群的紊乱,CD4+ CD28-T细胞及CD8+ CD22-T细胞的异常增高可能参与了其发病过程,但与HSP临床类型无关.     

特发性血小板减少性紫癜患者CD3^＋、CD4^＋和CD8^＋T淋巴细胞凋亡率的研究

目的:通过检测CD3+、CD4+、CD8+T淋巴细胞的凋亡率,探讨T淋巴细胞凋亡在特发性血小板减少性紫癜(ITP)免疫发病机制中的作用。方法:应用流式细胞仪检测ITP患者外周血CD3+、CD4+、CD8+T淋巴细胞的凋亡率;分离ITP患者和正常人外周血单个核细胞(PBMC),分成A、B 2组,A组加入白介素2(IL-2),B组加入IL-2和地塞米松共培养,分别于24和48 h收获细胞,应用流式细胞仪检测CD3+、CD4+、CD8+T淋巴细胞的凋亡率。结果:①ITP患者组CD3+、CD4+、CD8+T淋巴细胞凋亡率均明显低于正常对照(均P<0.01);②细胞培养24 h时ITP患者组A、B 2组间CD3+、CD4+、CD8+T淋巴细胞凋亡率间均差异无统计学意义(均P>0.05),而48 h时B组CD3+、CD4+、CD8+T淋巴细胞的凋亡率均明显高于A组(P<0.05或0.01);正常对照组24和48 h B组CD3+、CD4+、CD8+T淋巴细胞凋亡率均明显高于A组(均P<0.05);③ITP患者组细胞培养24 h后A、B 2组间CD3+、CD4+、CD8+T淋巴细胞凋亡率的差值均明显低于正常对照组(P<0....     

免疫性血小板减少性紫癜35例患者外周血免疫细胞亚群的检测及其临床意义

目的 探讨免疫细胞亚群的变化在免疫性血小板减少性紫癜(ITP)发病机制中的作用及其临床意义.方法 应用流式细胞术检测35例ITP患者治疗前、后及20例正常对照者免疫细胞亚群各指标的变化,包括CD3+、CD4+、CD8+、CD56+、CD19+淋巴细胞及CD4+/CD8+比值.结果 ITP患者CD3+ T淋巴细胞百分比(61.58±6.45)%、CD4+ T淋巴细胞百分比(28.38±4.89)%、CD4+/CD8+比值(0.99±0.22)较对照组[(67.85±4.68)%、(38.00±3.37)%、1.54±0.13]均减低(P值均＜0.05),治疗后3项指标[(69.41±5.03)%、(38.17±3.18)%、1.60±0.15]均升高至正常水平;CD8+ T淋巴细胞百分比(29.20±4.50)%及CD19+ B淋巴细胞百分比(17.74±4.14)%较对照组[(24.82±2.93)%、(12.09±3.51)%]升高(P值均＜0.05),治疗后2项指标[(24.06±3.02)%、(10.90±3.55)%]均降至正常水平;ITP患者CD56+细胞百分比治疗前(15.80±2.85)%、治疗后(15.16±2.77)%与对照组(16.36±2.75)%差异无统计学意义(P＞0.05).结论 免疫细胞亚群紊乱参与了ITP的发病,对其检测可作为ITP的辅助诊断,在指导治疗方面可能有一定的意义.

Abstract：

Objective To explore the clinical significance of immunocyte subsets before and after immunosuppressive therapy in the peripheral blood of patients with immune thrombocytopenic purpura (ITP).MethodsThe percentages of immunocyte subsets in the peripheral blood of 35 patients with ITP and 20 healthy controls were detected by flow cytometry,including CD3+,CD4+,CD8+,CD56+,CD19+ lymphocytes and CD4+/CD8+.Results The percentages of CD3+ T lymphocyte (61.58 ± 6.45 ) %,CD4+ T lymphocyte (28.38 ±4.89)% and the ratio of CD4+/CD8+ 0.99 0.22 in patients with ITP were lower than those in healthy controls[( 67.85 ± 4.68 ) %,( 38.00 ± 3.37 ) %,1.54 ± 0.13,all P ＜ 0.05].After immunosuppressive therapy,the percentages of CD3+ T lymphocyte ( 69.41 ± 5.03 ) %,CD4+ T lymphocyte (38.17 ±3.18)% and the ratio of CD4+/CD8+ 1.60 ±0.15 recovered to control levels.The percentages of CD8+ T lymphocyte (29.20 ±4.50)% and CD19+B lymphocyte ( 17.74 ±4.14)% were higher than those in healthy controls[( 24.82 ± 2.93 ) % and ( 12.09 ± 3.51 ) %,all P ＜ 0.05].After the immunosuppressive therapy,the percentages of CD8+ T lymphocyte ( 24.06 ± 3.02 ) % and CD19+ B lymphocyte ( 10.90 ± 3.55 ) %recovered to control levels.There were no significant difference of the percentage of CD56+ lymphocyte among ITP patients ( 15.80 ± 2.85 )%,ITP patients after immunosuppressive therapy ( 15.16 ± 2.77 )% and healthy controls ( 16.36 ± 2.75 ) %.ConclusionThe aberrant immunocyte subsets are involved in the pathogenesis of ITP,and detection of immunocyte subsets might be helpful for the diagnosis and determination of therapeutic outcome of ITP.     

Expression of costimulatory molecules on peripheral blood lymphocytes of patients with systemic lupus erythematosus

OBJECTIVE: In systemic lupus erythematosus (SLE) autoantibody production is T cell dependent. For a proper T and B cell interaction, signalling of costimulatory molecules on these cells is necessary. The expression of costimulatory molecules on peripheral blood lymphocytes in patients with SLE in conjunction with disease activity was measured to evaluate whether expression of costimulatory molecules in SLE is increased. METHODS: Thirteen patients with SLE with active disease, 10 patients with inactive disease, and 14 controls entered the study. In addition, samples from 10 of the 13 patients with active disease could be studied at a moment of inactive disease as well. Isolated peripheral blood lymphocytes were stained for the lymphocyte subset markers CD4, CD8, CD19, their respective activation markers CD25, HLA-DR, CD38, and the costimulatory molecules CD40L, CD28, CD40, CD80, and CD86. Expression was measured by flow cytometry. RESULTS: Peripheral blood lymphocytes of patients with SLE showed signs of increased activation at the moment of active disease. Almost all CD4+ T cells expressed CD28, both in patients and in controls. CD80 expression on CD19+ B cells was low in both groups and did not correlate with disease activity. In contrast, the percentage of CD19+ B cells expressing CD86 was increased in patients with SLE even in patients with inactive disease (p=0.04) and correlated with the SLEDAI score (p=0.0005) and levels of anti-dsDNA (p=0.006). No changes in CD40 or CD40L expression were found in the patients with SLE. CONCLUSION: In patients with SLE the expression of CD86 on CD19+ B cells is increased and is associated with disease activity, B cell activation, and levels of anti-dsDNA. The increased CD86 expression will render (autoreactive) B cells more susceptible for T cells. This can facilitate autoantibody production and might be a target for immunosuppressive treatments.     

Effect of irinotecan on the phenotype of peripheral blood leukocyte populations in patients with metastatic colorectal cancer

BACKGROUND/AIMS: Previous studies have demonstrated a significant decrease in absolute numbers of CD3+CD4+, CD8+CD28+ and CD19+ lymphocytes, and an increase in the expression of activation markers on T-cells and the number of CD14+CD16+ monocytes in patients with metastatic cancer. Irinotecan (CPT-11) is now being widely used for treatment of metastatic colorectal cancer patients. METHODOLOGY: We have examined, by two-color flow cytometry, peripheral blood leukocyte populations before and during systemic treatment with CPT-11 in 14 patients with metastatic colorectal cancer. RESULTS: CD3+, CD3+CD4+, CD3+CD8+, CD8+CD28+ and CD19+ were significantly lower, and CD3+HLA-DR+ and CD14+CD16+ cells were higher in metastatic colorectal cancer patients compared to controls. After 2-4 months of CPT-11-based chemotherapy, significant increase in CD3+CD4+ cell numbers was observed in 8 patients who had initial CD3+CD4+ counts of less than 600 per microL (358 +/- 154 vs. 652 +/- 319 cells per microL, Wilcoxon test, P < 0.01), while in patients with higher initial CD3+CD4+ counts a trend for decrease was observed during therapy. A trend for an increase in CD8+CD28+ cell counts was observed in patients with low CD3+CD4+ numbers, but no other changes were observed during the treatment in other peripheral blood leukocyte populations examined. CONCLUSIONS: CD3+CD4+ lymphocytopenia, a decrease in CD8+CD28+ and CD19+ lymphocytes, increased expression of activation markers and CD14+CD16+ monocytosis are present in a significant proportion of metastatic colorectal cancer patients. CPT-11-based therapy seems to ameliorate CD3+CD4+ lymphocytopenia, possibly by neutralizing the immunosuppressive effects of uncontrolled tumor growth. These observations may be useful for the design of immunotherapy trials in metastatic colorectal cancer.     

Proinflammatory mediator-induced reversal of CD4+,CD25+ regulatory T cell-mediated suppression in rheumatoid arthritis

OBJECTIVE: We previously demonstrated that CD4+,CD25+ regulatory T (Treg) cells are present in increased numbers in the synovial fluid (SF) of rheumatoid arthritis (RA) patients and display enhanced suppressive activity as compared with their peripheral blood (PB) counterparts. Despite the presence of these immunoregulatory cells in RA, chronic inflammation persists. The purpose of the present study was to investigate whether particular proinflammatory mediators that are associated with RA could abrogate CD4+,CD25+ Treg-mediated suppression. METHODS: Monocyte phenotype was determined by flow cytometry and cytokine levels by enzyme-linked immunosorbent assay. Magnetically sorted CD4+,CD25- and CD4+,CD25+ T cells derived from the PB and SF obtained from RA patients were stimulated alone or in coculture with anti-CD3 monoclonal antibody (mAb) and autologous antigen-presenting cells, in the absence or presence of anti-CD28 mAb or the proinflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor alpha (TNFalpha), or IL-7. RESULTS: Monocytes from the SF of RA patients displayed increased expression of HLA class II molecules, CD80, CD86, and CD40 as compared with PB-derived monocytes, indicating their activated status. Mimicking this increased costimulatory potential, addition of anti-CD28 mAb to cocultures of CD4+,CD25- and CD4+,CD25+ T cells resulted in reduced CD4+,CD25+ Treg-mediated suppression in both PB and SF. Furthermore, IL-7 and, to a limited extent, TNFalpha, both of which are produced by activated monocytes and were detected in SF, abrogated the CD4+,CD25+ Treg-mediated suppression. In contrast, IL-6 did not influence Treg-mediated suppression. CONCLUSION: Our findings suggest that the interaction of CD4+,CD25+ Treg cells with activated monocytes in the joint might lead to diminished suppressive activity of CD4+,CD25+ Treg cells in vivo, thus contributing to the chronic inflammation in RA.     

Lymphocyte subpopulations in peripheral blood in primary sclerosing cholangitis

BACKGROUND/AIMS: Primary sclerosing cholangitis (PSC) is a chronic disease of autoimmunological etiology, leading to inflammation, destruction and atrophy of the bile ducts. The aim of the study was to determine peripheral lymphocyte B, T, and NK cells in PSC. METHODOLOGY: The estimation of peripheral blood lymphocytes in 17 patients (54+/-12 years old) with PSC was carried out; the control group consisted of 27 subjects (38+/-11 years). The following T lymphocyte subpopulations were determined using duo color flow cytometry: CD3+, CD4+, CD8+, CD3++HLA DR+, B cells CD19+, and NK cells CD16+ +CD56+. RESULTS: In PSC we observed doubled increase in activated T lymphocytes of CD3+ +HLA DR+ phenotype as compared to healthy subjects (7.9% vs. 2.7%, p<0.01) and NK cells (12.6% vs. 10.3%, respectively, p<0.05). There were no significant differences in the composition of CD3+, CD4+, and CD8+. In peripheral blood we noted, in patients with PSC, a decrease in B lymphocytes (11.2% vs. 12.3%, p<0.19). CONCLUSIONS: The examinations showed that activated T (HLA DR+) lymphocytes and NK cells played an important role in development of PSC.     

CD28-T细胞亚群在类风湿关节炎患者外周血和关节液中的表达

目的 探讨CD28-T细胞亚群在类风湿关节炎(RA)患者外周血和关节液中的变化和意义。方法 随机选择RA患者45例,取新鲜抗凝外周血单个核细胞(PBMC),其中15例同时提取关节液单个核细胞( SFMC),以流式细胞技术检测CD28-T细胞数量及其表面可诱导共刺激分子(ICOS)的表达。2 组间比较用独立样本t检验。结果 ①与PBMC相比,RA患者SFMC中CD4+CD28+ ICOS+、CD4+CD28-ICOS+、CD8+ CD28+、CD8+ CD28+ ICOS+T细胞明显升高[(36±19)％与(15±8)％,t=-4.234,P＜0.01;(2.1±2.2)％与(0.6±1.4)％,t=-3.143,P＜0.01;(62±15)％与(47±18)％,t=-2.885,P＜0.01;(9±9)％与(3±3)％,t=-2.131,P＜0.05];CD8+CD28-T细胞明显降低[(38±15)％与(54±18)％,t=2.975,P＜0.01];CD8+ CD28- ICOS+、C1D4+CD28+和CD4+CD28-T细胞无明显变化（P＞0.05）。②同一RA患者SFMC与PBMC相比,CD4+CD28+ICOS+、CD8+ CD28+T细胞明显升高[(38±18)％与(16±10)％,t=-4.065,P＜0.01;(61±16)％与(41±21)％,t=-2.883,P＜0.01];CD8+ CD28-T细胞明显降低[(39±16)％与(59±21)％,t=2.949,P＜0.01]。③缓解期与活动期RA患者相比,PBMC中CD4+CD28-、CD8+ CD28-、CD28-ICOS+T细胞无明显变化（P＞0.05）。结论 RA患者关节液中CD28-T细胞亚群失衡和ICOS分子表达异常,可能是导致RA关节损伤的重要机制。     

Early activation of peripheral lymphocytes in human acute pancreatitis

BACKGROUND: The CD69 antigen is an indicator of early lymphocyte activation. GOALS: To evaluate the early activation of peripheral lymphocytes T, B, and NK in patients with acute pancreatitis in comparison with patients with acute abdomen of nonpancreatic origin. STUDY: Thirty patients with acute pancreatitis were studied; 20 of them had the mild form of the disease and 10 had the severe form. Thirty patients with nonpancreatic acute abdomen were used as controls. All patients were enrolled within 48 hours of the onset of pain. In all patients, leukocytes and total lymphocyte and lymphocyte subset counts (CD4+, CD8+, CD56+, CD19+, CD4+CD69+, CD8+CD69+, CD56+CD69+, CD19+CD69+) were determined upon hospital admission. RESULTS: The percentage of total lymphocytes was significantly lower in acute pancreatitis patients than in those with nonpancreatic acute abdomen (P = 0.014); patients with severe pancreatitis had a percentage of total lymphocytes significantly lower when compared with patients with mild pancreatitis (P < 0.001). The CD19+CD69+ count was significantly lower in patients with severe pancreatitis (24.6 +/- 14.6%) than in patients with mild pancreatitis (46.7 +/- 16.5%; = 0.006). The counts of the other lymphocyte subsets were not statistically different between patients with acute pancreatitis and those with nonpancreatic acute abdomen, as well as between patients with mild and severe acute pancreatitis. CONCLUSIONS: Patients with severe pancreatitis show impaired early activation of peripheral CD19+ cells.