IL-21/IL-21R信号在TNBS诱导小鼠炎症性肠病病变形成中的作用研究

被引：0
|
作者：
姜雪峰 [1 ]
贾楠 [1 ]
岳丹 [1 ,2 ]
王媛媛 [3 ]
张晓清 [1 ]
孙逊 [1 ]
机构：
[1] 中国医科大学基础医学院免疫学教研室
[2] 中国医科大学附属盛京医院检验科
[3] 中国医科大学附属第四医院麻醉科
来源：
微生物学杂志 | 2019年 / 39卷 / 01期
关键词：
IL-21/IL-21R信号; TNBS诱导的肠炎模型; Th1; Th2; Th17; Treg;
D O I：
暂无
中图分类号：
R574 [肠疾病];
学科分类号：
摘要：
探讨IL-21/IL21R信号在炎症性肠病病变形成中对肠固有层辅助T细胞应答的调控机制。利用IL-21R基因敲除小鼠(IL-21R KO),建立TNBS诱导的炎症性肠病动物模型。监测小鼠体重及生存率;HE染色观察小鼠肠组织形态结构及炎症反应情况;分离和提取肠固有层淋巴细胞(lamina propria lymphocyte,LPL),应用流式细胞仪检测Th1、Th2、Th17、Treg细胞比例和绝对数;ELISA法检测LPL培养上清中的细胞因子(IFN-γ、IL-4、IL-17A、IL-10)的分泌。结果显示:与WT小鼠相比,IL-21R KO小鼠体重下降更快,生存率明显降低;HE染色显示IL-21R KO小鼠肠管上皮损伤严重、隐窝大面积消失、大量炎性细胞浸润,并侵犯到黏膜肌层;IL-21R KO小鼠肠固有层Th1细胞应答显著增强,相反Th2、Th17和Treg应答明显抑制。因此,IL-21/IL-21R信号通过调节小鼠肠固有层Th细胞应答,在TNBS诱导的肠炎病变形成中发挥重要的保护性作用。
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页码：77 / 83
页数：7
相关论文
共 11 条
  • [1] Interleukin-21 Receptor Deficiency Increases the Initial Toll-like Receptor 2 Response but Protects Against Joint Pathology by Reducing Th1 and Th17 Cells During Streptococcal Cell Wall Arthritis
    Marijnissen, Renoud J.
    Roeleveld, Debbie M.
    Young, Deborah
    Nickerson-Nutter, Cheryl
    Abdollahi-Roodsaz, Shahla
    de Aquino, Sabrina Garcia
    van de Loo, Fons A. J.
    van Spriel, Annemiek B.
    Boots, Annemieke M. H.
    van den Berg, Wim B.
    Koenders, Marije I.
    [J]. ARTHRITIS & RHEUMATOLOGY, 2014, 66 (04) : 886 - 895
  • [2] Early-onset inflammatory bowel disease and common variable immunodeficiency–like disease caused by IL-21 deficiency.[J].Elisabeth Salzer;Aydan Kansu;Heiko Sic;Peter Májek;Aydan Ikincioğullari;Figen E. Dogu;Nina Kathrin Prengemann;Elisangela Santos-Valente;Winfried F. Pickl;Ivan Bilic;Sol A Ban;Zarife Kuloğlu;Arzu Meltem Demir;Arzu Ensari;Jacques Colinge;Marta Rizzi;Hermann Eibel;Kaan Boztug.The Journal of Allergy and Clinical Immunology.2014, 6
  • [3] Role of interleukin-21 isoform in dextran sulfate sodium (DSS)-induced colitis
    Araki, Akemi
    Nara, Hidetoshi
    Rahman, Mizanur
    Onoda, Tadashi
    Li, Jun
    Juliana, Farha Matin
    Jin, Lianjin
    Murata, Kazuko
    Takeda, Yuji
    Asao, Hironobu
    [J]. CYTOKINE, 2013, 62 (02) : 262 - 271
  • [4] IL-17 and Th17 Cells.[J].Thomas Korn;Estelle Bettelli;Mohamed Oukka;Vijay K. Kuchroo.Annual Review of Immunology.2009, 1
  • [5] A critical role of CD30 ligand/CD30 in controlling inflammatory bowel diseases in mice
    Sun, Xun
    Somada, Shinichi
    Shibata, Kensuke
    Muta, Hiromi
    Yamada, Hisakata
    Yoshihara, Hirofumi
    Honda, Kuniomi
    Nakamura, Kazuhiko
    Takayanagi, Ryhoichi
    Tani, Kenzaburo
    Podack, Eckhard R.
    Yoshikai, Yasunobu
    [J]. GASTROENTEROLOGY, 2008, 134 (02) : 447 - 458
  • [6] Regulation of gut inflammation and TH17 cell response by interleukin-21
    Fina, Damele
    Sarra, Massimiliano
    Fantini, Massimo C.
    Rizzo, Angelamaria
    Caruso, Roberta
    Caprioli, Flavio
    Stolfi, Carmine
    Cardolini, Iris
    Boirivant, Monica
    Pallone, Francesco
    MacDonald, Thomas T.
    Monteleone, Giovanni
    [J]. GASTROENTEROLOGY, 2008, 134 (04) : A256 - A256
  • [7] Functional Dynamics of Naturally Occurring Regulatory T Cells in Health and Autoimmunity.[J].Megan K. Levings;Sarah Allan;Eva d'Hennezel;Ciriaco A. Piccirillo.Advances in Immunology.2006,
  • [8] REGULATION OF TH2 DIFFERENTIATION AND Il4 LOCUS ACCESSIBILITY.[J].K. Mark Ansel;Ivana Djuretic;Bogdan Tanasa;Anjana Rao.Annual Review of Immunology.2006, 0
  • [9] Interleukin-21 enhances T-helper cell type I signaling and interferon-γ production in Crohn’s disease.[J].Giovanni Monteleone;Ivan Monteleone;Daniele Fina;Piero Vavassori;Giovanna Del Vecchio Blanco;Roberta Caruso;Roberto Tersigni;Luciano Alessandroni;Livia Biancone;Gian Carlo Naccari;Thomas T. MacDonald;Francesco Pallone.Gastroenterology.2005, 3
  • [10] Interleukin-21 triggers effector cell responses in the gut.[J].Daniela De Nitto;Massimiliano Sarra;Francesco Pallone;Giovanni Monteleone;.World Journal of Gastroenterology.2010, 29
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