共查询到20条相似文献，搜索用时 31 毫秒
1.
Rosas-Ballina M Olofsson PS Ochani M Valdés-Ferrer SI Levine YA Reardon C Tusche MW Pavlov VA Andersson U Chavan S Mak TW Tracey KJ 《Science (New York, N.Y.)》2011,334(6052):98-101
Neural circuits regulate cytokine production to prevent potentially damaging inflammation. A prototypical vagus nerve circuit, the inflammatory reflex, inhibits tumor necrosis factor-α production in spleen by a mechanism requiring acetylcholine signaling through the α7 nicotinic acetylcholine receptor expressed on cytokine-producing macrophages. Nerve fibers in spleen lack the enzymatic machinery necessary for acetylcholine production; therefore, how does this neural circuit terminate in cholinergic signaling? We identified an acetylcholine-producing, memory phenotype T cell population in mice that is integral to the inflammatory reflex. These acetylcholine-producing T cells are required for inhibition of cytokine production by vagus nerve stimulation. Thus, action potentials originating in the vagus nerve regulate T cells, which in turn produce the neurotransmitter, acetylcholine, required to control innate immune responses. 相似文献
2.
The TLR Expression Pattern on Monocyte-Derived Macrophages for Lipopolysaccharid Stimulation of Calves 总被引：1，自引：0，他引：1
GUO Yi-jie ZHAO Guo-Qi HUO Yong-jiu Sachi Tana-ka Hisashi Aso Takahiro Yamaguchi 《中国农业科学(英文版)》2009,8(7):864-871
In this paper, toll-like receptor expression pattern in monocytes-derived macrophages by lipopolysaccharid （LPS） stimulation was examined. Jugular venous blood samples from 4 Japanese calves were obtained and the peripheral blood mononuclear cells （PBMC） were isolated. The PBMC were cultured for 7 d so as to collect monocytes-derived macrophages in Repcell. The PBMC were stimulated by LPS for 24 h and the mRNA expression pattern of TLR and cytokines in monocytes-derived macrophages （Mod-Mφ） was analyzed. Results showed that LPS stimulation of Mod-Mφ could increase the mRNA levels of the genes of TNF-α, IL-6, and IL-8. In addition, the mRNA levels of the genes of TNF-α and IL-6 in the group of LPS stimulation were most significantly （P 〈 0.01） higher than those in control group and the mRNA levels of TLR1, 3, 5, 8, and 10 were significantly （P 〈 0.05） decreased after LPS stimulation. There was no difference in the mRNA expressions of TLR2, 4, 6, and 7 between the groups of the control and LPS stimulation. Besides, expression of TLR9 was not found. It suggested that monocytes-derived macrophages could respond to LPS and they might take an important role in the innate immunity. The important function of the cells might contribute to better disease treatment. 相似文献
3.
【目的】流感病毒感染引发机体的炎症反应及免疫稳态失衡，由此产生的细胞因子风暴（CS）是引起感染宿主死亡的主要原因。通过探究苦参碱对H9N2 AIV感染小鼠的保护作用及其调节NLRP3炎性体信号通路的特点及作用机制，可进一步完善中药抗病毒的理论依据，为新型抗病毒药物的研发奠定基础。【方法】72只8周龄BALB/c小鼠随机分为空白组（0.1 mL无菌鸡胚尿囊液）、病毒组（0.1 mL 4×105PFU/mLH9N2 AIV）、金刚烷胺组（0.1 mL 4×105PFU/mLH9N2 AIV+100×10-6 99%金刚烷胺）、苦参碱高浓度治疗组（0.1 mL 4×105PFU/mLH9N2 AIV+40 mL·kg-1苦参碱）、中浓度治疗组（0.1 mL 4×105PFU/mLH9N2 AIV+20 mL·kg-1苦参碱）和低浓度治疗组（0.1 mL 4×105PFU/mLH9N2 AIV+10 mL·kg-1苦参碱），每组12只，含病毒鸡胚尿囊液滴鼻构建小鼠病毒性肺炎模型，灌服或饮水给药治疗连续5 d，试验共进行7 d，观察不同组小鼠的体重变化。在第1、3、5、7天分别取3只小鼠无菌采血并处死，取小鼠肺组织进行病理组织学观察，RT-PCR检测小鼠肺组织中H9N2 NA、NLRP3 NLR基因表达情况，Western Blot检测苦参碱治疗后H9N2感染小鼠肺组织NLRP3炎性体信号通路相关蛋白表达量的变化，小鼠血清用ELISA法测定细胞因子TNF-α、IL-1β和IL-10表达量的变化。【结果】与病毒组相比，苦参碱高浓度治疗组病理组织学观察中H9N2 AIV感染小鼠肺部水肿的区域明显减少，红细胞渗出减少，炎性细胞数量减少，效果接近金刚烷胺组。7 d时苦参碱高浓度治疗组小鼠肺泡壁完好，肺泡之间分界清楚，肺组织内炎性细胞、浆细胞数量大量减少，与空白组无异;苦参碱中浓度治疗组肺组织少量出血，肺泡内无渗出液，肺泡间隔完好;苦参碱低浓度治疗组可见肺泡内红细胞渗出，大量浆细胞募集，肺泡之间出现融合现象。经过苦参碱和金刚烷胺治疗的各组小鼠肺组织中H9N2病毒基因表达量在3、5和7 d极显著降低（P<0.01）。经治疗3、5 d时，苦参碱高浓度治疗组和金刚烷胺组的NLRP3基因和蛋白表达量、TNF-α、IL-1β蛋白表达量极显著降低（P<0.01）;7 d时，苦参碱高、中、低治疗组小鼠肺组织中NLRP3基因表达量极显著降低（P<0.01）;5 d时苦参碱低浓度治疗组NLRP3蛋白、Caspase-1蛋白和中浓度组Caspase-1蛋白表达量显著降低（P<0.05）;3 d、5 d时苦参碱中、低浓度治疗组TNF-α和IL-1β蛋白表达量极显著降低（P<0.01），苦参碱中浓度治疗组IL-10表达量极显著降低。【结论】苦参碱可在体内抑制H9N2 AIV的表达，通过下调NLRP3炎性体信号通路相关蛋白，下调TNF-α、IL-1β和IL-10的表达，减轻炎症反应，有良好的抗病毒、抗炎作用。 相似文献
4.
Nancy P Tagliani E Tay CS Asp P Levy DE Erlebacher A 《Science (New York, N.Y.)》2012,336(6086):1317-1321
The chemokine-mediated recruitment of effector T cells to sites of inflammation is a central feature of the immune response. The extent to which chemokine expression levels are limited by the intrinsic developmental characteristics of a tissue has remained unexplored. We show in mice that effector T cells cannot accumulate within the decidua, the specialized stromal tissue encapsulating the fetus and placenta. Impaired accumulation was in part attributable to the epigenetic silencing of key T cell-attracting inflammatory chemokine genes in decidual stromal cells, as evidenced by promoter accrual of repressive histone marks. These findings give insight into mechanisms of fetomaternal immune tolerance, as well as reveal the epigenetic modification of tissue stromal cells as a modality for limiting effector T cell trafficking. 相似文献
5.
Anderson AC Anderson DE Bregoli L Hastings WD Kassam N Lei C Chandwaskar R Karman J Su EW Hirashima M Bruce JN Kane LP Kuchroo VK Hafler DA 《Science (New York, N.Y.)》2007,318(5853):1141-1143
CD4+ T helper 1 (TH1) cells are important mediators of inflammation and are regulated by numerous pathways, including the negative immune receptor Tim-3. We found that Tim-3 is constitutively expressed on cells of the innate immune system in both mice and humans, and that it can synergize with Toll-like receptors. Moreover, an antibody agonist of Tim-3 acted as an adjuvant during induced immune responses, and Tim-3 ligation induced distinct signaling events in T cells and dendritic cells; the latter finding could explain the apparent divergent functions of Tim-3 in these cell types. Thus, by virtue of differential expression on innate versus adaptive immune cells, Tim-3 can either promote or terminate TH1 immunity and may be able to influence a range of inflammatory conditions. 相似文献
6.
目的研究白细胞介素-12（Interleukin 12,IL-12）对小鼠S180实体瘤的抗肿瘤作用并初步探讨其机制.方法将小鼠左后肢皮下接种S180细胞荷瘤后的BaLB/c小鼠随机分为生理盐水组和IL-12组,分别给予生理盐水和IL-12.接种第28天,眼球取血,流式细胞仪分析外周血T细胞亚群的变化;解剖取瘤称重,计... 相似文献
7.
【目的】通过测定先天性免疫效应因子分泌水平的变化,研究鼠李糖乳杆菌（Lactobacillus rhamnosus）体外对巨噬细胞先天性免疫应答调节的影响。【方法】将培养好的鼠巨噬细胞系RAW264.7细胞分为4组,分别用PBS（CT组,对照组）、Escherichia coli K88（EC组）和Lactobacillus rhamnosus（LR组）处理12 h,以及先用Lactobacillus rhamnosus预处理1 h,再用Escherichia coli K88处理12 h（LR-EC组）。试验结束时,收集各组的细胞培养液,用ELISA检测TNF-α、IFN-γ、IL-1β、IL-6、IL-12、IL-8、IL-10,以及PGE2和 的含量。【结果】结果表明,CT组（对照组）可产生TNF-α、IFN-γ、IL-8和IL-10,几乎不产生IL-1β、IL-6和IL-12。与对照组相比,EC组TNF-α、IFN-γ、IL-8、IL-10及PGE2和 含量均极显著提高（P＜0.01）,且可大量产生IL-1β、IL-6和IL-12;LR组TNF-α、IFN-γ、IL-10及PGE2和 也极显著提高（P＜0.01）,IL-8显著增加（P＜0.05）,同样不产生IL-1β和IL-6,但可产生微量的IL-12（P＜0.01）;LR-EC组所有的促炎细胞因子（TNF-α、IFN-γ、IL-1β、IL-6、IL-12）、趋化因子IL-8和PGE2均极显著高于EC组（P＜0.01）,但IL-10和 含量都显著低于EC组（P＜0.01）。【结论】在体外试验条件下,鼠李糖乳杆菌作为益生菌对生理状态下巨噬细胞先天性免疫应答的刺激作用远低于病原菌,不会产生炎症反应,但可极大增强受感染巨噬细胞的促炎免疫应答水平,且可能具有避免过度炎症反应的作用。 相似文献
8.
Mucida D Park Y Kim G Turovskaya O Scott I Kronenberg M Cheroutre H 《Science (New York, N.Y.)》2007,317(5835):256-260
The cytokine transforming growth factor-beta (TGF-beta) converts na?ve T cells into regulatory T (Treg) cells that prevent autoimmunity. However, in the presence of interleukin-6 (IL-6), TGF-beta has also been found to promote the differentiation of na?ve T lymphocytes into proinflammatory IL-17 cytokine-producing T helper 17 (T(H)17) cells, which promote autoimmunity and inflammation. This raises the question of how TGF-beta can generate such distinct outcomes. We identified the vitamin A metabolite retinoic acid as a key regulator of TGF-beta-dependent immune responses, capable of inhibiting the IL-6-driven induction of proinflammatory T(H)17 cells and promoting anti-inflammatory Treg cell differentiation. These findings indicate that a common metabolite can regulate the balance between pro- and anti-inflammatory immunity. 相似文献
9.
[目的]探讨miR-155在脂多糖(LPS)诱导的RAW264.7巨噬细胞炎症反应中的表达及糖皮质激素(GCs)的干预影响。[方法]体外培养RAW 264.7巨噬细胞,分别用浓度为10.0、1.0、0.1μg/ml LPS刺激RAW 264.7巨噬细胞,于2、6、12、24、36 h 5个时间点收集上清用ELISA检测白介素-6(IL-6)蛋白浓度;实时定量-PCR检测miR-155在2、6、12、36 h 4个时间点的表达变化。[结果]IL-6在各浓度LPS处理组、各时间点其含量均高于对照组(CK);miR-155的表达在各时间点LPS组均高于LPS+GCs和CK。[结论]LPS可以诱导RAW264.7巨噬细胞的炎症反应,炎症反应时miR-155高表达,糖皮质激素可抑制miR-155的表达。 相似文献
10.
Zhu Z Zheng T Homer RJ Kim YK Chen NY Cohn L Hamid Q Elias JA 《Science (New York, N.Y.)》2004,304(5677):1678-1682
Chitin is a surface component of parasites and insects, and chitinases are induced in lower life forms during infections with these agents. Although chitin itself does not exist in humans, chitinases are present in the human genome. We show here that acidic mammalian chitinase (AMCase) is induced via a T helper-2 (Th2)-specific, interleukin-13 (IL-13)-mediated pathway in epithelial cells and macrophages in an aeroallergen asthma model and expressed in exaggerated quantities in human asthma. AMCase neutralization ameliorated Th2 inflammation and airway hyperresponsiveness, in part by inhibiting IL-13 pathway activation and chemokine induction. AMCase may thus be an important mediator of IL-13-induced responses in Th2-dominated disorders such as asthma. 相似文献
11.
Interleukin-1 mitogenic activity for fibroblasts and smooth muscle cells is due to PDGF-AA 总被引：57，自引：0，他引：57
Both interleukin-1 (IL-1) and platelet-derived growth factor (PDGF) induce proliferation of cultured fibroblasts and smooth muscle cells. These polypeptide mediators are released by activated macrophages and other cell types in response to injury and are thought to have a role in tissue remodeling and a number of pathologic processes. Analysis of the kinetics of [3H]thymidine incorporation by cultured fibroblasts demonstrated that the response to IL-1 is delayed approximately 8 hours relative to their response to PDGF. IL-1 transiently stimulated expression of the PDGF A-chain gene, with maximum induction after approximately 2 hours. Subsequent synthesis and release of PDGF activity into the medium was detected as early as 4 hours after IL-1 stimulation, and downregulation of the binding site for the PDGF-AA isoform of PDGF followed PDGF-AA secretion. Antibodies to PDGF completely block the mitogenic response to IL-1. Therefore, the mitogenic activity of IL-1 for fibroblasts and smooth muscle cells appears to be indirect and mediated by induction of the PDGF A-chain gene. 相似文献
12.
In a study of the relation between chronic inflammation and carcinogenesis, C3H mouse fibroblasts of the 10T 1/2 clone 8 line (10T 1/2 cells) were exposed to human neutrophils stimulated to synthesize reactive oxygen intermediates or to a cell-free enzymatic system generating superoxide (xanthine oxidase plus hypoxanthine). After exposure, the 10T 1/2 cells were either placed in tissue culture or immediately injected into athymic nude mice. Both malignant and benign tumors developed in the mice injected with treated cells, but not in those injected with control cells; in one instance cells grown from one of the benign tumors subsequently developed a malignant phenotype. Malignant transformation was also observed in treated cells in the experiments in vitro. 相似文献
13.
[目的]研究NH4＋引起炎症反应的机制。[方法]利用倒置显微镜观察不同盐离子引起单核癌细胞THP-1形态的变化,乳酸脱氢酶（LDH）试剂盒检测细胞培养上清中LDH,台盼蓝染色检测细胞形态和存活情况,Western blot检测炎症反应相关细胞因子的产生和分泌。[结果]通过体外研究发现NH4＋能够激活caspase-1和下游的IL-1β,IL-1β是炎症反应的重要细胞因子;K＋能够抑制NH4＋引起的caspase-1和IL-1β的激活。[结论]Na＋、SO24-、Cl-都不引起炎症反应,对THP-1细胞没有影响;NH4＋能够引起单核细胞的炎症反应,并且可以被K＋抑制,为氨基酸代谢紊乱引起的疾病的治疗提供了一定的依据。 相似文献
14.
【目的】探讨猪伪狂犬病毒（Pseudorabies virus,PRV）感染对小鼠单核巨噬细胞（RAW264.7）炎症反应的影响,确定PRV的最佳感染剂量和感染时间,为建立RAW264.7细胞体外病毒感染炎症反应模型打下基础。【方法】PRV按10倍递增稀释成10-5~10-1 PRV稀释液,感染RAW264.7细胞并孵育1.5 h,弃病毒液后加入含5%胎牛血清的DMEM维持培养液继续培养,分别于继续培养2、4、8、12、24和48 h时收集细胞上清液,采用ELISA测定IL-6、IL-10、IL-1β、TNF-α、MCP-1和IFN-γ分泌水平及环氧合酶（COX-1和COX-2）活性,并以CCK-8法测定细胞活性。【结果】以PRV感染RAW264.7细胞4~48 h后均能通过PCR扩增获得PRV核酸的特异性条带,故选择4~48 h作为后续研究的PRV感染时间范围;10-2 PRV~10-1 PRV感染可显著降低RAW264.7细胞活性（P<0.05,下同）,10-3 PRV组仅在培养48 h时出现下降趋势,而10-5 PRV~10-4 PRV感染对RAW264.7细胞活性无显著影响。PRV感染RAW264.7细胞后,其胞内炎症因子IL-6、IFN-γ、TNF-α、IL-1β和MCP-1的分泌水平整体上呈升高趋势,其中10-3 PRV感染RAW264.7细胞12 h能显著或极显著（P<0.01）提高IL-6、IFN-γ、TNF-α、IL-1β和MCP-1的分泌水平;10-4 PRV~10-1 PRV感染组的IL-10分泌水平均呈升高趋势,而10-5 PRV感染组在感染8和24 h时IL-10分泌水平明显低于空白对照组,至感染48 h所有病毒感染组的IL-10分泌水平均降低;10-3 PRV~10-1 PRV感染8~24 h能有效提高RAW264.7细胞的COX-2活性,但对COX-1活性的影响不明显。【结论】PRV感染能诱导RAW264.7细胞发生炎症反应,其中10-3 PRV体外感染RAW264.7细胞8~12 h是建立RAW264.7细胞炎症反应模型的最佳条件。该模型可应用于PRV感染与RAW264.7细胞炎症反应相关干预药物的研究,为进一步揭示PRV感染机理及开发抗病毒感染药物提供理论依据。 相似文献
15.
【目的】探讨松针多糖对鸡巨噬细胞HD11的天然免疫功能的影响,以期为松针多糖在肉鸡疾病防治方面应用提供科学依据。【方法】试验采用不同浓度的的松针多糖作用于巨噬细胞HD11,试验分为空白对照组、阳性对照组（终浓度为1 μg·mL-1的LPS）和松针多糖组（终浓度分别为25、50、100、200、400 μg·mL-1的松针多糖）。噻唑蓝（MTT）检测巨噬细胞HD11细胞活性、Griess法检测巨噬细胞HD11细胞上清液中一氧化氮（NO）分泌量、中性红吞噬试验检测巨噬细胞HD11吞噬活性,酶联免疫（ELISA）检测巨噬细胞HD11细胞上清液中干扰素-α（IFN-α）、一氧化氮合酶（iNOS）、白介素-10（IL-10）、白介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的含量,荧光定量PCR技术检测HD11细胞中iNOS mRNA表达。【结果】 MTT试验结果表明：与空白对照组相比,不同浓度的松针多糖（25、50、100、200、400 μg·mL-1）对细胞活性没有影响,说明在25-400 μg·mL-1范围内对巨噬细胞没有毒性,可以进行免疫调节作用实验。免疫调节作用试验结果表明：与空白对照组相比,不同浓度的松针多糖极显著（P<0.01）增加了NO释放量和细胞吞噬活性,极显著（P<0.01）或显著（P<0.05）提高了细胞因子IFN-α的含量和iNOS的含量及mRNA的表达量,极显著（P<0.01）或显著（P<0.05）降低了细胞因子IL-10的分泌量。当松针多糖浓度在50、100、200、400 μg·mL-1浓度时,细胞因子IL-6和TNF-α的含量极显著（P<0.01）高于空白对照组。与阳性对照组相比,不同浓度的松针多糖极显著（P<0.01）降低NO释放量,极显著（P<0.01）或显著（P<0.05）降低了细胞因子IFN-α的含量、iNOS的含量及mRNA表达量和IL-10含量。当松针多糖浓度在25、50、100 μg·mL-1浓度时,细胞吞噬活性极显著（P<0.01）低于阳性对照组,细胞因子IL-6的含量极显著（P<0.01）低于阳性对照组。当松针多糖浓度在25、50、100、200 μg·mL-1浓度时,细胞因子TFN-α的含量极显著（P<0.01）低于阳性对照组。【结论】松针多糖能显著提高巨噬细胞HD11的天然免疫调节能力,且存在剂量依赖效应。 相似文献
16.
[目的]建立猪繁殖与呼吸综合征病毒(PRRSV)诱导体内猪肺泡巨噬细胞(PAM)炎症模型,评价PRRSV感染对仔猪免疫系统的影响,为猪繁殖与呼吸综合征(PRRS)的临床诊断及科学防控提供参考依据.[方法]以PRRSV-GXNN1396株人工感染30日龄健康断奶仔猪,复制出PRRS病症,剖杀后采集病料,通过组织病理学和RT-PCR检测观察各免疫器官组织的病理变化及其病毒分布情况,并检测PAM细胞内的COX-1、COX-2等酶活性变化及IL-6、IL-8、IL-10、IL-1β、IFN-γ、MCP-1和TNF-α等炎性细胞因子水平变化.[结果]断奶仔猪接种PRRSV-GXNN1396株后第3d开始表现出典型的PRRS病症,PRRSV主要集中在肺脏、颌下淋巴结、血液和扁桃体等样品组织中,攻毒仔猪各主要器官的实质细胞及有关淋巴细胞均出现不同程度坏死和炎症细胞浸入现象,尤其以肺脏、肾脏、脾脏等器官受损严重,出现巨噬细胞和淋巴细胞浸润.PRRSV感染早期(第3d)仔猪PAM细胞中的ROS水平及COX-2、IL-6、IL-8、IL-10和TNF-α等因子水平均呈升高趋势,且COX-2、IL-6、IL-8和TNF-α因子水平极显著升高(P<0.01);随着感染天数的增加,PAM细胞内的COX-2、IL-6和IL-8因子水平呈下降趋势,TNF-α因子水平呈上升趋势.[结论]成功建立了PRRSV诱导仔猪体内PAM细胞炎症模型,进一步佐证PRRSV主要侵害猪的免疫器官组织,以达到免疫抑制的效果,并推断感染第3d是病猪炎症反应的高峰期. 相似文献
17.
LPS与ATP共同诱导巨噬细胞中NLRP3炎症小体的激活 总被引：1，自引：0，他引：1
【目的】以脂多糖(LPS)为刺激源,探索小鼠巨噬细胞(RAW264.7)中NOD样受体家族pyrin结构域蛋白3(NLRP3)炎性小体激活的响应机制。【方法】试验分为对照组、LPS组、LPS与ATP共同刺激组。ELISA检测NLRP3源性白介素-1β(IL-1β)表达情况;RT-PCR检测NLRP3、Caspase-1、白介素-1β(IL-1β)的转录水平;ELISA检测LPS与NLRP3其他激动剂(MSU、CPPD、SiO2、Alum)共同作用后IL-1β的表达以及PI染色检测细胞焦亡。【结果】与对照组相比,LPS刺激组对IL-1β的表达无显著影响,LPS/ATP共同刺激组IL-1β的表达显著升高;LPS/ATP刺激组NLRP3、Caspase-1、IL-1βmRNA的表达显著升高且LPS/ATP刺激组发生明显的细胞焦亡。【结论】LPS与ATP共同作用能够显著提高NLRP3、Caspase-1、IL-1β的表达,说明LPS对NLRP3炎性小体的激活是LPS与ATP共同作用实现的。 相似文献
18.
CX3CR1-mediated dendritic cell access to the intestinal lumen and bacterial clearance 总被引：3，自引：0，他引：3
Niess JH Brand S Gu X Landsman L Jung S McCormick BA Vyas JM Boes M Ploegh HL Fox JG Littman DR Reinecker HC 《Science (New York, N.Y.)》2005,307(5707):254-258
Dendritic cells (DCs) and macrophages are critical to innate and adaptive immunity to the intestinal bacterial microbiota. Here, we identify a myeloid-derived mucosal DC in mice, which populates the entire lamina propria of the small intestine. Lamina propria DCs were found to depend on the chemokine receptor CX3CR1 to form transepithelial dendrites, which enable the cells to directly sample luminal antigens. CX3CR1 was also found to control the clearance of entero-invasive pathogens by DCs. Thus, CX3CR1-dependent processes, which control host interactions of specialized DCs with commensal and pathogenic bacteria, may regulate immunological tolerance and inflammation. 相似文献
19.
Identification of a T helper cell-derived lymphokine that activates resting T lymphocytes 总被引：3，自引：0，他引：3
A novel lymphokine with apparent molecular size of 10 to 12 kilodaltons is secreted from helper T cell clones within hours after cross-linking their T cell antigen-MHC (major histocompatibility complex) receptors (T3-Ti). This lymphokine, termed interleukin-4A (IL-4A), stimulates resting lymphocytes by binding to a surface component (or components) of the alternative T11 pathway and subsequently by inducing interleukin-2 (IL-2) receptors. The activation process is neither dependent on antigen specificities of the recruited population or the presence of macrophages. It appears, therefore, that IL-4A is a mediator involved in amplifying the T cell immune response. 相似文献
20.
【目的】观察猪圆环病毒2型（PCV-2）感染对猪肾传代细胞（PK-15细胞）炎性细胞因子白细胞介素（IL） mRNA转录水平的影响,探讨宿主与病毒之间的作用关系及细胞炎性反应机制。【方法】以未感染PCV-2的PK-15细胞为对照组,运用相对定量PCR技术,测定和分析PCV2感染PK15细胞后,PCV-2 DNA相对含量的变化,以及炎性细胞因子IL-6、IL-8、IL-12p35、IL-12p40、IL-13、IL-17、IL-18 mRNA转录水平在1,6,12,24,48,和72 h的变化。【结果】PCV-2感染后,PK-15细胞的IL-6、IL-13、IL-17、IL-18 的mRNA转录水平在12 h显著增加,24 h后mRNA转录水平下降;IL-8的mRNA转录水平在48 h时最高,为对照组的2.5倍,但72 h时恢复至与对照组水平相当;随着感染时间的延长,IL-12p35、IL-12p40 的mRNA转录水平显著下降。【结论】PCV-2感染后可引起PK-15细胞中IL-6、IL-8、IL-13、IL-17、IL-18等细胞因子mRNA转录水平增加,而IL-12 mRNA转录水平下降,提示PCV-2感染后引起的PK-15细胞炎性反应与其分泌的炎性细胞因子的改变有关。 相似文献