>
网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
T细胞CD28家族受体在哮喘发病中的作用
作者:许雪梅  唐宗生  李志鸿 
单位:皖南医学院弋矶山医院 儿科, 安徽 芜湖 241000
关键词:白细胞分化抗原28 可诱导共刺激分子 细胞毒性T淋巴细胞抗原-4 程序性死亡受体-1 B和T淋巴细胞弱化因子 哮喘 综述 
分类号:R562.25
出版年·卷·期(页码):2016·35·第六期(1009-1013)
摘要:

哮喘是儿童常见的慢性呼吸系统疾病,患病人数多,上升快。关于哮喘发病机制研究众多。研究认为共刺激分子CD28-B7-1/B7-2、ICOS-ICOSL、CTLA-4-B7-1/B7-2、PD-1-PDL-1/PDL-2、BTLA-HVEM 5条共刺激信号通路主要影响T细胞的活化、增殖和分化,并导致Th1/Th2分化比例失衡,在过敏性疾病和哮喘的发病过程中起重要作用。本文作者综合叙述有关T细胞CD28家族受体在哮喘发病中的作用。

参考文献:

[1] MASOLI M,FABIAN D,HOLT S,et al.The global burden of asthma:executive summary of the GINA dissemination committee report[J].Allergy,2004,59(5):469-478.
[2] ASHER M I,MONTEFORT S,BJÖRKSTÉN B,et al.Worldwide time trends in the prevalence of symptoms of asthma,allergic rhinoconjunctivitis,and eczema in childhood:ISAAC phases one and three repeat multicountry cross-sectional surveys[J].Lancet,2006,368(9537):733-743.
[3] CHEN Y,WONG G W,LI J.Environmental exposure and genetic predisposition as risk factors for asthma in China[J].Allergy Asthma Immunol Res,2016,8(2):92-100.
[4] JUNG D Y,LEEM J H,KIM H C,et al.Effect of traffic-related air pollution on allergic disease:results of the children's health and environmental research[J].Allergy Asthma Immunol Res,2015,7(4):359-366.
[5] BRANDT E B,MYERS J M,RYAN P H,et al.Air pollution and allergic diseases[J].Curr Opin Pediatr,2015,27(6):724-735.
[6] TSE K,HORNER A A.Allergen tolerance versus the allergic march:the hygiene hypothesis revisited[J].Curr Allergy Asthma Rep,2008,8(6):475-483.
[7] 卢旭.支气管哮喘患儿的危险因素分析[J].现代医学,2011,39(4):417-418.
[8] GOGISHVILI T,LVHDER F,KIRSTEIN F,et al.Interruption of CD28-mediated costimulation during allergen challenge protects mice from allergic airway disease[J].J Allergy Clin Immunol,2012,130(6):1394-1403.
[9] 林昭鹂,尹玉敏.儿童哮喘致病因素探讨[J].现代医学,2005,33(3):191-192.
[10] ASAI-TAJIRI Y,MATSUMOTO K,FUKUYAMA S,et al.Small interfering RNA against CD86 during allergen challenge blocks experimental allergic asthma[J].Respir Res,2014,15(1):132.
[11] LI J G,DU Y M,YAN Z D,et al.CD80 and CD86knockdown in dendritic cells regulates Th1/Th2 cytokine production in asthmatic mice[J].Exp Ther Med,2016,11(3):878-884.
[12] DONG C,JUEDES A E,Temann U A,et al.ICOS co-stimulatory receptor is essential for T-cell activation and function[J].Nature,2001,409(6816):97-101.
[13] KADKHODA K,WANG S,FAN Y,et al.ICOS ligand expression is essential for allergic airway hyperresponsiveness[J].Int Immunol,2011,23(4):239-249.
[14] AKBARI O,FREEMAN G J,MEYER E H,et al.Antigen-specific regulatory T cells develop via the ICOS-ICOS-ligand pathway and inhibit allergen-induced airway hyperreactivity[J].Nat Med,2002,8(9):1024-1032.
[15] 谢琼.IL-10基因-627C/A多态性与儿童哮喘病之间的相关性研究[J].现代医学,2012,40(1):51-53.
[16] BAUQUET A T,JIN H,PATERSON A M,et al.The costimulatory molecule ICOS regulates the expression of c-maf and IL-21 in the development of follicular T helper cells and Th-17 cells[J].Nat Immunol,2009,10(2):167-175.
[17] LICONA-LIMÓN P,KIM L K,PALM N W,et al.Th2,allergy and group 2 innate lymphoid cells[J].Nat Immunol,2013,14(6):536-542.
[18] MAAZI H,AKBARI O.ICOS regulates ILC2s in asthma[J].Oncotarget,2015,6(28):24584-24585.
[19] HOWARD T D,POSTMA D S,HAWKINS G A,et al.Fine mapping of an IgE-controlling gene on chromosome 2q:Analysis of CTLA4 and CD28[J].J Allergy Clin Immunol,2002,110(5):743-751.
[20] LEE S Y,LEE Y H,SHIN C,et al.Association of asthma severity and bronchial hyperresponsiveness with a polymorphism in the cytotoxic T-lymphocyte antigen-4 gene[J].Chest,2002,122(1):171-176.
[21] YAO Y S,WANG L H,CHANG W W,et al.Association between CTLA-4 exon-1+49A/G polymorphism and asthma:an updated meta-analysis[J].Int J Clin Exp Med,2015,8(3):3107-3113.
[22] LINHART B,BIGENZAHN S,HARTL A,et al.Costimulation blockade inhibits allergic sensitization but does not affect established allergy in a murine model of grass pollen allergy[J].J Immunol,2007,178(6):3924-3931.
[23] MAAZI H,SHIRINBAK S,DEN BOEF L E,et al.Cytotoxic T lymphocyte antigen 4-immunoglobulin G is a potent adjuvant for experimental allergen immunotherapy[J].Clin Exp Immunol,2013,172(1):113-120.
[24] AKBARI O,STOCK P,SINGH A K,et al.PD-L1 and PD-L2 modulate airway inflammation and iNKT-cell-dependent airway hyperreactivity in opposing directions[J].Mucosal Immunol,2010,3(1):81-91.
[25] MATSUMOTO K,INOUE H,NAKANO T,et al.B7-DC regulates asthmatic response by an IFN-gamma-dependent mechanism[J].J Immunol,2004,172(4):2530-2541.
[26] MCALEES J W,LAJOIE S,DIENGER K,et al.Differential control of CD4(+)T-cell subsets by the PD-1/PD-L1 axis in a mouse model of allergic asthma[J].Eur J Immunol,2015,45(4):1019-1029.
[27] OFLAZOGLU E,SWART D A,ANDERS-BARTHOLO P,et al.Paradoxical role of programmed death-1 ligand 2 in Th2 immune responses in vitro and in a mouse asthma model in vivo[J].Eur J Immunol,2004,34(12):3326-3336.
[28] YEE L J,PEREZ K A,TANG J,et al.Association of CTLA-4 polymorphisms with sustained response to interferon and ribavirin therapy for chronic hepatitis C virus infection[J].J Infect Dis,2003,187(8):1264-1271.
[29] DEPPONG C,JUEHNE T I,HURCHLA M,et al.Cutting edge:B and T lymphocyte attenuator and programmed death receptor-1 inhibitory receptors are required for termination of acute allergic airway inflammation[J].J Immunol,2006,176(7):3909-3913.
[30] WARE C F,SEDY J.New isolated herpesvirus entry mediator polypeptide variant useful in pharmaceutical composition for treating an inflammatory disease e.g. lupus and asthma,specifically binds B and T lymphocyte attenuator and does not bind CD 160:America,WO2013074738-A1[P].2013-05-23.
[31] SHUBIN N J,CHUNG C S,HEFFERNAN D S,et al.BTLA expression contributes to septic morbidity and mortality by inducing innate inflammatory cell dysfunction[J].J Leukoc Biol,2012,92(3):593-603.

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 418279 位访问者


copyright ©《东南大学学报(医学版)》编辑部
联系电话:025-83272481 83272483
电子邮件:
bjb@pub.seu.edu.cn

苏ICP备09058364