红毛五加多糖对体外正常人T淋巴细胞转化增殖的促进作用

目的:研究红毛五加多糖对体外正常人外周血淋巴细胞活性的影响.方法:采用MTr比色法监测正常人外周血T淋巴细胞活性.结果:AGP1,AGP2 and AGP3组OD值分别是0.80±0.03、0.73±0.01 and 0.67±0.02,AGP1、AGP2组与对照组相比有统计学差异(P＜0.05).结论:红毛五加多糖对体外PHA诱导的正常人外周血T淋巴细胞的增殖有促进作用(P＜0.05),可能是一种免疫增强剂.     

红景天多糖对体外正常人T淋巴细胞活性和体外人胃癌细胞增殖的影响(英文)

目的研究红景天多糖对体外正常人T淋巴细胞活性和对体外人胃癌细胞增殖的影响。方法采用MTT比色法和体外细胞培养计数法。结果红景天多糖对体外PHA诱导的正常人外周血T淋巴细胞的增殖有显著性促进作用(P<0.05);红景天多糖对体外人胃癌细胞增殖有显著性抑制作用(P<0.05),且红景天多糖作用强于香菇多糖(P<0.05)。结论红景天多糖可能是一种免疫增强剂,对胃癌可能有一定防治作用。     

淋巴细胞亚群功能状态的影响

目的:探讨黄芪注射液对银屑病患者辅助性T淋巴细胞(Th细胞)亚群功能状态的影响.方法:对20 例银屑病患者的外周血淋巴细胞体外分别经植物血凝素(PHA)和PHA+黄芪诱导:即病例对照组和病例黄芪组,同时对10 例健康志愿者外周血淋巴细胞体外经PHA诱导(即正常对照组),各组培养48 h,用ELISA法检测培养上清液中Th类细胞因子IFN-γ和IL-4含量.结果:病例对照组IFN-γ水平高于正常对照组(P＜0.05),而IL-4水平低于正常对照组(P＜0.05).病例黄芪组IFN-γ水平低于病例对照组(P＜0.05),而IL-4水平高于病例对照组(P＜0.05).结论:黄芪注射液可显著下调银屑病患者Th1亚群优势状态,促进向Th2亚群转换,改善患者Th1/Th2失衡状态,对银屑病的治疗具有重要意义.     

来氟米特对系统性红斑狼疮T淋巴细胞的免疫调节作用

目的探讨来氟米特(LEF)在体外对系统性红斑狼疮(SLE)患者外周血T淋巴细胞的免疫调节作用。方法在植物血凝素(PHA)刺激下,SLE患者外周血T淋巴细胞与不同浓度的LEF5、15、45μg/ml共培养。检测各组T淋巴细胞的增殖、凋亡情况,分析各组T淋巴细胞免疫表型CD152、CD28的表达以及各组T淋巴细胞的干扰素(IFN)γ、白细胞介素(IL)10、转化生长因子(TGF)β1 mRNA水平。结果在体外,LEF对由PHA诱导的SLE患者T淋巴细胞的增殖、凋亡均有抑制作用,且抑制作用与LEF呈剂量依赖性。LEF对T淋巴细胞CD152、CD28的表达无明显影响。LEF促进IL-10、TGF-β1 mRNA的表达,抑制IFN-γ mRNA的表达。结论 LEF可能通过减少T淋巴细胞凋亡、促进T淋巴细胞分泌IL-10、TGF-β1以及减少T淋巴细胞分泌IFN-γ来下调SLE的免疫反应。     

红景天多糖对老年小鼠TLC亚群及IL-2的影响

目的:研究红景天多糖对老年小鼠TLC亚群及IL-2的影响,探讨中药红景天多糖在老年小鼠免疫功能调节方面的作用机制。方法:应用流式细胞技术、放射免疫方法检测老年小鼠T淋巴细胞亚群,外周血白介素-2(IL-2)含量。结果:红景天多糖对老年小鼠T淋巴细胞亚群、外周血IL-2含量均有增强作用(P<0.05)。结论:红景天多糖能够提高老年小鼠的免疫功能,是一种良好的抗衰老中药。     

羧甲基茯苓多糖和PHA诱导人外周血淋巴细胞产生GM-CSF的研究

健康人外周血淋巴细胞在羧甲基茯苓多糖与PHA等的刺激诱导下共同培养7d后可获高效价粒-巨噬细胞集落刺激因子。该制剂经特殊处理后可达到临床药用标准。     

人树突状细胞融合肝癌细胞体外诱导特异性抗肿瘤免疫

目的 探讨人树突状细胞(DC)融合肝癌细胞(HCC)体外诱导T淋巴细胞产生特异性抗肝癌免疫的作用.方法 应用人重组粒细胞/巨噬细胞集落刺激因子(rhGM-CSF)和重组人白细胞介素4(rhIL-4)对人外周血单个核细胞进行体外诱导产生树突状细胞,流式细胞仪检测DC表面标志物表达水平,聚乙二醇融合DC与肝癌细胞HerG2,MTT法测定融合细胞(HerG2/DC)刺激T淋巴细胞增生、分化能力,细胞毒性实验检测HerG2/DC诱导的细胞毒T淋巴细胞(CTL)对HerG2的特异性杀伤作用.结果 融合细胞HerG2/DC刺激T淋巴细胞增值能力明显提高,HerG2/DC活化的CTL对HerG2具有明显的特异性杀伤作用.结论 人树突状细胞融合肝癌细胞可有效诱导T淋巴细胞产生特异性的抗肝癌肿瘤免疫.     

不同体外诱导物对T细胞疫苗诱导免疫耐受作用的影响

目的 :探讨不同的疫苗细胞体外诱导物对 T细胞疫苗 ( TVC)诱导免疫耐受作用的影响 ,方法 :用 L OU /C大鼠脾细胞免疫 BN大鼠 ,取免疫过的 BN大鼠脾细胞进行淋巴细胞转化实验 ,计算刺激指数 ( SI) ,比较 Con A和PHA两种诱导物对 T细胞的诱导增殖作用 ;用被 L OU/C大鼠抗原活化的 BN大鼠脾细胞作为疫苗细胞 ,在体外经Con A诱导增殖后灭活制备 TCV1、经 PH诱导增殖后灭活制备 TCV2 ,用制备的 T细胞疫苗分别免疫正常的 BN大鼠 ,于免疫后进行单向混合淋巴细胞反应 ( ML R) ,计算抑制率。结果 :淋巴细胞转化实验 :Con A的 SI为 2 1.4 2 ,显著高于 PHA的 SI( 4 .93) ( P<0 .0 1) ;ML R:TCV1免疫组抑制率为 87.75 % ,TCV2免疫组抑制率为 34.6 6 % ,与 TCV1免疫组比较 P<0 .0 1。结论 :用 Con A诱导的疫苗细胞制备的 T细胞疫苗 ,可以显著抑制被免疫大鼠脾细胞的免疫应答能力 ,体外诱导物的诱导增殖作用越大 ,所制备的 T细胞疫苗诱导免疫耐受的能力越强     

测定白细胞介素2活性的一种简单微量法

作者根据白细胞介素2(IL-2)能激发带IL-2受体的人外周白细胞增殖,介绍一种改良的微量测定法。作者用重组IL-2(rIL-2)和由混合淋巴细胞反应(MLR)产生的含有IL-2的上清液,诱导依赖IL-2鼠细胞毒性T细胞系(BD2.10)、依赖IL-2的人T细胞系(NO.9)、植物血凝素(PHA)激活的人T细胞以及在含10%胎牛血清或自体血清的培养液中培养10天的人外周血单个核细胞即“训练细胞”(educated cell)的增殖。通过~3H-胸苷掺入测定细胞增     

灵芝多糖和当归多糖促进人外周血T淋巴细胞增殖和分泌IFN-γ

目的探讨中药灵芝多糖和当归多糖对人外周血活化T淋巴细胞的免疫调节作用。方法分离健康人外周血T淋巴细胞并分为空白对照组、灵芝多糖组和当归多糖组,免疫荧光观察各组T细胞PI3K和Caspase-3蛋白的表达;MTT法检测培养72 h后各组T细胞的增殖水平;流式细胞术分析各组T细胞凋亡率和细胞周期变化;ELISA检测各组T细胞培养上清液的IFN-γ含量。结果灵芝多糖组和当归多糖组T细胞均表达PI3K,细胞增殖OD值均明显高于空白对照组(P<0.01,P<0.05);灵芝多糖组T细胞Caspase-3蛋白表达的平均光密度值明显低于空白对照组(P<0.05),T细胞凋亡率也低于空白对照组,分别为18.23%和29.74%;灵芝多糖组和当归多糖组T细胞培养上清液IFN-γ的含量明显高于空白对照组(P<0.05,P<0.05)。结论灵芝多糖和当归多糖均明显促进外周血T淋巴细胞增殖和分泌IFN-γ,灵芝多糖还能下调Caspase-3蛋白表达并抑制T淋巴细胞凋亡。     

腺苷对细胞免疫功能的影响

腺苷１３，１３０ｍｇ·ｋｇ－１抑制小鼠的迟发型超敏反应，１０，１００，１０００μｍｏｌ·Ｌ－１抑制小鼠外周全血的淋巴细胞增殖反应，脾淋巴细胞增殖反应和小鼠脾细胞产生白细胞介素２。在人外周血淋巴细胞转化反应中１０００μｍｏｌ·Ｌ－１才可见明显的抑制作用；氨茶碱２２μｍｏｌ·Ｌ－１逆转１０００μｍｏｌ·Ｌ－１的作用，潘生丁１０μｍｏｌ·Ｌ－１部分逆转１０００μｍｏｌ·Ｌ－１的作用，提示腺苷可能通过腺苷受体而起作用。     

Effect of lead exposure on the immune response of some occupationally exposed individuals

Lead is a ubiquitous pollutant in the industrial environment, which poses serious threats to human health. In the past 20 years increasing attention has been paid to the effects of lead exposure on health. This toxic metal alters the immune response of animals as well as humans. To study the immunological effects of occupational exposure to lead, we examined lymphocyte proliferation, natural killer (NK) cell cytotoxicity and interferon-gamma production with peripheral blood mononuclear cells (PBMCs) of individuals occupationally exposed to lead. We selected three different groups of individuals exposed to lead: three-wheeler drivers (30), battery workers (34) and silver jewelery makers (20); and unexposed healthy volunteers (30) as control for comparison. Our results indicate that though lymphocyte proliferation to phytohaemagglutinin (PHA) is inhibited in lead exposed individuals as compared with unexposed volunteers, there is no correlation between inhibition of lymphocyte proliferation and blood lead level. NK cell cytotoxicity remains unaffected in individuals exposed to lead as compared with controls. On the other hand, we observed that interferon-gamma (IFN-gamma) was significantly elevated in T cell mitogen, PHA, stimulated PBMCs culture supernatant of lead exposed individuals. We found significant positive correlation between blood lead levels and IFN-gamma produced in culture supernatant on stimulation with PHA. In brief, this study demonstrates that lead can affect the immune response of the occupationally exposed individuals such as three-wheeler drivers, battery reconditioning workers and silver jewelery makers.     

Synthesis and immunotropic properties of 5-substituted 1,5-benzodiazepin-2-ones derivatives in cultures of human peripheral blood cells, Part III

The reaction of 4-methyl-(A) and 3-methyl-1H-2,3,4,5-tetrahydro-1,5-benzodiazepin-2-one (B) with selected alpha,beta-unsaturated acid chlorides: crotonoyl, cinnamoyl, and 4-nitrocinnamoyl is described. We have also characterized immunotropic activities of these compounds in the proliferative response of human lymphocytes to phytohemagglutinin A (PHA) or to allogeneic cells in one-way mixed lymphocyte reaction (MLR), as well as their action on tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) production in peripheral blood mononuclear cells (PBMC) and mixed lymphocyte cultures (MLC). Some of the compounds exhibited regulatory activities in the proliferative response of cells to PHA depending on the reactivity of cells to PHA. The MLR induced proliferation of lymphocytes was moderately inhibited by two selected compounds. The compounds showed also inhibitor properties with regard to lipopolysaccharide (LPS)- and MLR-induced TNF-alpha production. Structure-activity relationship was discussed.     

Helper T cell subpopulations from women are more susceptible to the toxic effect of sodium arsenite in vitro

Arsenic is known to produce inhibition as well as induction of proliferative responses in animal and human cells depending on the doses. Despite the amount of information on the immunotoxic effects of arsenic exposure in different animal models, little is known in humans. Arsenic susceptibility of lymphocyte subpopulations (T helper (Th), CD4+; T cytotoxic (Tc), CD8+) and whether arsenic effects are gender related are still to be determined. This work evaluated the in vitro toxicity of sodium arsenite on human T lymphocyte subpopulations from men and women. Peripheral blood mononuclear cells (PBMC) obtained from healthy young men and women were treated with sodium arsenite (0.01, 0.1, and 1 microM). We assessed cell viability, cell proliferation, and the proportion of Th and Tc cells after 48 or 72h of arsenic exposure in resting and phytohemagglutinin M (PHA)-activated PBMC. We observed that sodium arsenite at 1 microM was more toxic for Th than for Tc cells in PBMC from women. Besides, T lymphocytes from women were more affected by the cell proliferation inhibition induced by arsenic, suggesting that women could be more susceptible to the toxic and immunotoxic effects caused by arsenic exposure.     

苯并咪唑衍生物BM935抑制T细胞增殖的机制研究

目的探讨苯并咪唑衍生物BM935抑制人T细胞增殖的作用机制。方法流式细胞术检测细胞增殖、CD25表达及细胞周期。ELISA检测细胞培养上清IL-2含量。结果 BM935能抑制PHA或anti-CD3/CD28活化的T细胞增殖及混合淋巴细胞反应。BM935不抑制anti-CD3/CD28活化的T细胞产生IL-2和表达CD25,但将细胞周期阻滞在G0/G1期。结论 BM935通过阻滞细胞周期进程抑制T细胞增殖。BM935可以作为一种先导化合物用于开发新型免疫抑制剂。     

Immunological alterations induced by polyamine derivatives on murine splenocytes and human mononuclear cells

Three polyamine derivatives assigned as bis-naphthalimidopropyl putrescine (BNIPPut), spermidine (BNIPSpd) and spermine (BNIPSpm) were studied to determine their effects on the proliferation of murine splenocytes and human peripheral blood mononuclear cells (PBMC) induced by the mitogens, Con A, LPS and PHA. All compounds showed a dose dependent inhibitory effect on mouse and human T cell proliferation induced by the mitogens, with BNIPPut exhibiting the most potent antiproliferative activity, followed by BNIPSpd and by BNIPSpm, respectively (Put > Spd > Spm), when considering human T cells. This suppressive activity also affects the capacity of mouse spleen cells to produce Th1 cytokines, namely IL-2 and INF-gamma after in vitro stimulation with Con A. The polyamine-induced inhibition also occurred in the case of LPS-stimulated B cells with a marked decrease of CD69 expression by these cells. Furthermore, the ability for these polyamine derivatives to induce apoptosis on Con A-stimulated splenocytes could be related to their antiproliferative activity.     

青藤碱治疗类风湿性关节炎免疫作用和机制

目的研究青藤碱(sinomenine,SIN)对动物免疫功能和细胞凋亡的影响及对人滑膜细胞增殖影响。方法 MTT法测定脾淋巴细胞增殖反应及滑膜细胞增殖反应。采用流式细胞术测定脾T淋巴细胞亚型。流式细胞仪和DNA Ladder测定脾淋巴细胞凋亡。结果SIN在体给药抑制LPS及PMA诱导的小鼠脾淋巴细胞增殖。SIN离体给药可抑制ConA，LPS和anti-CD3 mAb诱导小鼠脾淋巴细胞增殖；SIN可使AA大鼠升高的CD4⁺/CD8⁺比值降低。SIN体外使小鼠脾淋巴细胞早期凋亡百分比显著增加。SIN对人类风湿关节炎滑膜细胞增殖也有抑制作用。结论 SIN对小鼠和类风湿关节炎大鼠脾淋巴细胞免疫功能具有抑制作用，诱导细胞凋亡可能是SIN免疫抑制作用的机理之一。     

Activation-induced T cell apoptosis by monocytes from stem cell products.

We recently found that mobilized peripheral blood stem cell (PSC) products (from both cancer patients and normal donors) contain high levels of CD14+ monocytes, which can inhibit the proliferation of allogeneic and autologous T cells. We found in our studies that using CD14+ monocytes from mobilized PSC products (from normal and cancer patient donors), normal apheresis products or normal peripheral blood (PB) can affect lymphocyte function and apoptosis-dependent T cell activation. However, it appears that the apoptosis is dependent on the frequency of monocytes, which is increased by both mobilization and apheresis. Both phytohemagglutinin (PHA)- and interleukin (IL)-2-induced proliferation of steady-state peripheral blood mononuclear cells (PBMC) were markedly inhibited by co-culture with irradiated CD14+ monocytes, although inhibition was significantly greater with PHA than with IL-2 stimulation. IL-2 (predominately CD56+ NK cells) or anti-CD3 monoclonal antibody (mAb) and IL-2-expanded lymphocytes (activated T cells) were inhibited by PSC monocytes to a significantly greater level as compared to steady-state lymphocytes. Indeed, no inhibition of T cell proliferation was observed when lymphocytes were co-cultured in the absence of mitogenic or IL-2 stimulation. In contrast, an increased proliferation was observed in co-cultures of CD14+ monocytes and steady-state or activated lymphocytes without mitogenic stimulation. Cell cycle analysis by flow cytometry revealed a significant increase in hypodiploid DNA, in a time-dependent manner, following co-culture of monocytes and PBMC in PHA, suggesting that T cell apoptosis occurred during PHA-induced activation. These results demonstrate that PSC-derived monocytes inhibit T cell proliferation by inducing the apoptosis of activated T cells and NK cells, but not steady-state cells. This suggests a potential role for monocytes in the induction of peripheral tolerance following stem cell transplantation.     

Suppressive effect of thymosin fraction 5 on proliferation of cultured human T lymphocytes

The effects of thymosin fraction 5 (F5), an extract of bovine thymus containing multiple polypeptides, on the proliferation of cultured T cells (CTC), a continuously proliferating subpopulation of peripheral blood T lymphocytes, stimulated by either phytohemagglutinin (PHA) or delectinated interleukin 2 (IL-2) were studied. Addition of F5 to cultures significantly and consistently inhibited CTC responsiveness to PHA, with the degree of inhibition being greater using a suboptimal concentration of mitogen. F5 did not significantly or consistently inhibit CTC proliferation induced by IL-2. These studies suggest that the suppressive effect of F5 may be primarily mediated by decreased IL-2 production instead of effects on IL-2 activity or efficiency in stimulating CTC proliferation. Since prostaglandins inhibit the proliferation of CTC in response to PHA or IL-2 (R.D. Maca (1983) Immunopharmacology 6:267), studies were undertaken to determine if the observed inhibition was mediated by effects of F5 on prostaglandin E2 (PGE2). The inhibitory effect of F5 on PHA responsiveness of CTC was not affected by the addition of indomethacin indicating that suppression by F5 is not mediated by stimulating the production or release of cyclooxygenase-derived prostaglandins, such as PGE2. Furthermore, PGE2 could not be detected in supernatants of F5-treated CTC stimulated by PHA. When PGE2 was added to F5-treated CTC cultures, the PHA response was inhibited indicating that the suppressive effects of F5 and PGE2 were additive and that F5 did not modulate the sensitivity of CTC to PGE2.(ABSTRACT TRUNCATED AT 250 WORDS)