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白细胞介素-33促进胶原诱导性关节炎的实验研究
  • ISSN号:1007-7480
  • 期刊名称:《中华风湿病学杂志》
  • 时间:0
  • 分类:R593.22[医药卫生—临床医学;医药卫生—内科学]
  • 作者机构:[1]北京大学人民医院风湿免疫科,100044, [2]英国格拉斯哥大学免疫系
  • 相关基金:国家973计划(2010cB529100);北京大学人民医院发展基金(RDB2008-23)
中文摘要:

目的探讨新型细胞因子白细胞介素(IL)-33在胶原诱导性关节炎(CIA)发病中的作用。方法建立DBA/1小鼠的CIA模型。以牛II型胶原(CII),完全福氏佐剂(CFA)免疫,从免疫后第21天开始每天注射IL-33或磷酸盐缓冲液(PBS)共5d。免疫后第28天取小鼠淋巴结细胞体外培养,培养上清的细胞因子浓度以酶联免疫吸附试验(ELISA)法检测或Luminex检测。同时检测血清中抗Ⅱ型胶原抗体和血清中的细胞因子浓度。鼠爪脱钙后行病理检查。采用两样本均数的t检验、r检验进行统计学处理。结果IL-33可使小鼠实验性的关节炎发病加重,致炎性细胞因子和抗Ⅱ型胶原抗体产生增多(P〈0.05),PBS组与IL-33组的IgG2a型Ⅱ型胶原抗体为[(1.24±0.33)mg/L和(1.96±0.16)mg/L,P〈0.05],而IgGl型抗Ⅱ型胶原抗体为[(1.1±0.4)mg/L和(1.7±0.4)mg/L,P〈0.05]。结论IL-33是炎性关节病中的重要致炎因子。这一IL-1家族新成员是潜在的类风湿关节炎(RA)治疗靶点。

英文摘要:

Objective To explore the role of a new cytokine interleukin (IL)-33 in collagen induced arthritis (CIA). Methods The murine model of CIA was employed. DBA/1 mice were immunized with C II/CFA and challenged with the same dose of CII in PBS on day 21. The mice were injected i.p daily with IL-33 or PBS for.5 days from day 21. Lymphonodes were removed on day 28 after primary immunization and cultured. The concentrations of all eytokines of the supernatants were determined by ELISA or an 20-plexmouse cyto-kine assay according to the manufacturer's instructions. Serum anti-C II antibody and mice paw histology were also assessed. Two indenpendent samples t test, chi-square test were used for statistical analysis. Results DBA/1 mice receiving 1L-33 injection exhibited an exacerbated CIA both in terms of clinical eyaluation and histological parameters. IL-17, IFN-γ, TNF-α, IL-5, IL-12, GM-CSF, MCP-1 and IP-10 productions were also elevated in IL-33 group (P〈0.05). Similarly, mice in the IL-33 injection group had higher levels of anti-collagen antibodies compared with those of the controls. The concentrations of C II - specific IgG2a were [(1.96±0.16) vs (1.24±0.33) mg/L] (P〈0.05), while IgG1 anti-C II antibodies were [ (1.1±0.4) vs (1.7±0.4) mg/L] (P〈0.05). Conclusion IL-33 is a critical pro-inflammatory cytokine for inflamm-atory joint disease. Thus this novel IL-1 superfamily member represents a novel therapeutic target for rheumatoid arthritis (RA).

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期刊信息
  • 《中华风湿病学杂志》
  • 中国科技核心期刊
  • 主管单位:中国科学技术协会
  • 主办单位:中华医学会
  • 主编:
  • 地址:山西省太原市东华门23号
  • 邮编:030013
  • 邮箱:cmafsb@163.com
  • 电话:0351-7553295 7553182
  • 国际标准刊号:ISSN:1007-7480
  • 国内统一刊号:ISSN:14-1217/R
  • 邮发代号:22-153
  • 获奖情况:
  • 1998年,《中华风湿病学杂志》社被共青团省委、山...,1999年获山西省第二届书刊装帧艺术作品一等奖,1999—2002年被评为山西省一级期刊
  • 国内外数据库收录:
  • 美国化学文摘(网络版),中国中国科技核心期刊,中国北大核心期刊(2008版),中国北大核心期刊(2011版),中国北大核心期刊(2014版)
  • 被引量:16745