CD4+CD25+Foxp3+调节性T细胞与IL-33在儿童哮喘发病机制中的作用

潘珍珍; 李羚; 郭赟; 贺建

doi:10.7499/j.issn.1008-8830.2014.12.005

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中国当代儿科杂志 ›› 2014, Vol. 16 ›› Issue (12) : 1211-1214. DOI: 10.7499/j.issn.1008-8830.2014.12.005

论著·临床研究

CD4⁺CD25⁺Foxp3⁺调节性T细胞与IL-33在儿童哮喘发病机制中的作用

潘珍珍, 李羚, 郭赟, 贺建

作者信息 +

Roles of CD4⁺CD25⁺Foxp3⁺ regulatory T cells and IL-33 in the pathogenesis of asthma in children

PAN Zhen-Zhen, LI Ling, GUO Yun, HE Jian

Author information +

文章历史 +

摘要

目的探讨CD4⁺CD25⁺Foxp3⁺调节性T细胞(Treg)与IL-33在儿童哮喘发病中的作用.方法采用流式细胞仪检测45例哮喘患儿(哮喘组)、50例呼吸道合胞病毒感染喘息患儿(喘息组)及40例健康儿童(对照组)外周血CD4⁺CD25⁺Foxp3⁺Treg细胞百分比,采用ELISA法检测各组外周血血清IFN-γ、IL-4、IL-5及IL-33浓度,进行比较分析.结果哮喘组患儿体内CD4⁺CD25⁺Foxp3⁺Treg 水平较喘息组及对照组均降低(P<0.05);哮喘组患儿体内IL-33水平较喘息组及对照组均升高(P<0.05),哮喘组患儿体内CD4⁺CD25⁺Foxp3⁺Treg与IL-33呈负相关(r=-0.156,P<0.01).结论在哮喘患儿发病机制中,CD4⁺CD25⁺Foxp3⁺Treg与IL-33可能存在相互作用.

Abstract

Objective To study the roles of CD4⁺CD25⁺Foxp3⁺ regulatory T cells (Treg) and IL-33 in the pathogenesis of asthma in children. Methods Flow cytometry was used to detect peripheral blood CD4⁺CD25⁺Foxp3⁺Treg proportion in CD4⁺T lymphocytes in.45 children with asthma, 50 children with wheezing caused by respiratory syncytial virus infection and 40 healthy children. Serum levels of IFN-γ, IL-4, IL-5 and IL-33 were measured using ELISA. Results The level of peripheral blood CD4⁺CD25⁺Foxp3⁺Treg in the asthma group was significantly lower than in the wheezing and control groups (P<0.05). In contrast, serum levels of IL-33 in the asthma group was significantly higher than in the wheezing and control groups (P<0.05). Peripheral blood CD4⁺CD25⁺Foxp3⁺Treg level was negatively correlated with serum IL-33 level in the asthma group(r=-0.156, P<0.01). Conclusions CD4⁺CD25⁺Foxp3⁺Treg may interact with IL-33 in the pathogenesis of childhood asthma.

导出引用

潘珍珍, 李羚, 郭赟, 贺建. CD4⁺CD25⁺Foxp3⁺调节性T细胞与IL-33在儿童哮喘发病机制中的作用[J]. 中国当代儿科杂志. 2014, 16(12): 1211-1214 https://doi.org/10.7499/j.issn.1008-8830.2014.12.005

PAN Zhen-Zhen, LI Ling, GUO Yun, HE Jian. Roles of CD4⁺CD25⁺Foxp3⁺ regulatory T cells and IL-33 in the pathogenesis of asthma in children[J]. Chinese Journal of Contemporary Pediatrics. 2014, 16(12): 1211-1214 https://doi.org/10.7499/j.issn.1008-8830.2014.12.005

参考文献

[1] Shimizu T, Kida Y, Kuwano K. TriacylaTed lipoproTeins derived from Mycoplasma pneumoniae acTivaTe nuclear facTor-kappa B Through Toll-like recepTors 1 and 2[J]. Immunology, 2007, 121(4): 473-483.
[2] 阳艳丽, 潘玉琴, 何帮顺, 等. 哮喘患儿外周血调节性T细胞和Th1/Th2的变化及其与哮喘病情的关系[J].中国当代儿科杂志, 2011, 13(6): 482-485.
[3] 康妍萌, 丁明杰, 韩玉玲, 等. 重症肺炎支原体肺炎患儿肺泡灌洗液中Th1/Th2细胞免疫应答状况的研究[J]. 中国当代儿科杂志, 2011, 13(3): 188-190.
[4] Zhang M, Qian YY, Chai SJ, eT al. Enhanced local Foxp3 expression in lung Tissue aTTenuaTes airway inflammaTion in a mouse model of asThma[J]. J AsThma, 2014, 51(5): 451-458.
[5] Hardy RD, Jafri HS, Olsen K, eT al. ElevaTed cyTokine and chemokine levels and prolonged pulmonary airflow resisTance in a murine Mycoplasma pneumoniae pneumonia model: a microbiologic, hisTologic, immunologic, and respiraTory pleThysmographic profile[J]. InfecT Immun, 2001, 69(6): 3869-3876.
[6] Baba S, Kondo K, Kanaya K, eT al. Expression of IL-33 and iTs recepTor ST2 in chronic rhinosinusiTis wiTh nasal polyps[J]. Laryngoscope, 2014, 124(4): E115-E122.
[7] STelmaszczyk-Emmel A, Zawadzka-Krajewska A, Szypowska A, eT al. Frequency and acTivaTion of CD4⁺CD25 Foxp3+ regulaTory T cells in peripheral blood from children wiTh aTopic allergy[J]. InT Arch Allergy Immunol, 2013, 162(1): 16-24.
[8] 魏明,涂玲, 梁颖红, 等. 臭氧暴露对CD4⁺CD25^highFoxp3⁺T调节性淋巴细胞数量和Foxp3 mRNA表达的影响[J]. 中华劳动卫生职业病杂志, 2013, 31(9): 693-696.
[9] Licona-Limón P, Kim LK, Palm NW, eT al. Th2, allergy and group 2 innaTe lymphoid cells[J]. NaT Immunol, 2013, 14(6): 536-542.
[10] Saglani S, Lui S, Ullmann N, eT al. IL-33 promoTes airway remodeling in pediaTric paTienTs wiTh severe sTeroid-resisTanT asThma[J]. J Allergy Clin Immunol, 2013, 132(3): 676-685.
[11] 麻晓燕, 罗雅玲, 赖文岩. 支气管哮喘患者外周血、痰液中IL-33的含量及其相关性分析[J]. 第三军医大学学报, 2011, 33(14): 1526-1529.
[12] Ayyoub M, Raffin C, Valmori D. GeneraTion of Th17 from human naive CD4⁺ T cells preferenTially occurs from FOXP3⁺ Tregs upon cosTimulaTion via CD28 or CD5[J]. Blood, 2012, 119(20): 4810-4812.