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Toll样受体3介导的信号通路在原发性胆汁性肝硬化模型中的作用

费允云 张文 高金明 刘斌 张奉春

中华临床免疫和变态反应杂志2011,Vol.5Issue(1):5-9,后插1,6.
中华临床免疫和变态反应杂志2011,Vol.5Issue(1):5-9,后插1,6.

Toll样受体3介导的信号通路在原发性胆汁性肝硬化模型中的作用

Role of Toll-Like Receptor 3 Signaling Pathways in the Induction of Primary Biliary Cirrhosis

费允云 1张文 1高金明 2刘斌 3张奉春1

作者信息

  • 1. 中国医学科学院,北京协和医学院,北京协和医院风湿免疫科,北京,100032
  • 2. 中国医学科学院,北京协和医学院,北京协和医院呼吸科,北京,100032
  • 3. 青岛大学医学院附属医院,山东青岛,266053
  • 折叠

摘要

Abstract

Objective To investigate whether TLR3 signaling pathway were involved in the pathogenesis of PBC.Methods Female C57BL/6 wide-type and CXCR3-/- mice were injected with 5 mg/kg of poly I:C intraperitoneally twice a week for 24 consecutive weeks. Liver specimens were collected to evaluate the degree of cell infiltration. Autoantibodies, including AMA, were assayed by ELISA. The liver expressions of TLR3 ,TRIF and p-NFKB p65 in mice model and control mice were evaluated by immunoblotting. Results The liver protein level of TLR3 was elevated in PBC mice. There was no significant difference in TLR3 level among different periods or between wide-type (WT) mice and CXCR3-/- mice. The level of TLR3 wasdecreased in PBC CXCR3-/- mice of 16 weeks and 24 weeks period. There was no significant difference in TRIF level between PBC mice and control mice or between WT mice and CXCR3-/- mice. There was no significant difference of p-NFκB p65 level between PBC mice and control mice. The level of p-NFκB p65 in CXCR3-/- PBC mice was higher than control, which was increased evidently over 16 weeks period.Conclusions TLR3 signaling pathway might be involved in the pathogenesis of PBC mice. NF-κB might not be the key transcription factor in the development of PBC. CXCR3 have no great effect on TLR3 signaling pathways in the induction of PBC.

关键词

原发性胆汁性肝硬化/趋化因子受体3/Toll样受体3/TIR区域的调节分子1/核因子κB

Key words

primary biliard cirrhosis / chemokine receptor 3 / toll-like receptor 3 / TRIF / nuclear factor-κB

分类

医药卫生

引用本文复制引用

费允云,张文,高金明,刘斌,张奉春..Toll样受体3介导的信号通路在原发性胆汁性肝硬化模型中的作用[J].中华临床免疫和变态反应杂志,2011,5(1):5-9,后插1,6.

基金项目

国家十一五科技支撑计划(2008BAI59B03),国家自然科学基金(30470767) (2008BAI59B03)

中华临床免疫和变态反应杂志

OACSTPCD

1673-8705

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