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干扰素-γ对Graves病甲状腺细胞凋亡的影响 被引量:3

Effects of IFN-γ on the apoptosis of thyrocytes from patients with Graves' disease
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摘要 目的探讨干扰素-γ(interferon-γ,IFN-γ)对Graves病(GD)患者甲状腺细胞凋亡的影响。方法取5例GD患者甲状腺组织,采用原代细胞培养技术、细胞增殖实验和流式细胞术检测IFN-γ对甲状腺细胞增殖活力、细胞凋亡率以及对Fas蛋白表达率的影响,应用ELISA检测IFN-γ刺激甲状腺细胞后培养上清液中sFas含量的变化。结果与未加IFN-γ处理的对照组相比,经IFN-γ处理的甲状腺细胞增殖活力明显降低(P<0.05),但甲状腺细胞的凋亡率、Fas蛋白表达率以及培养上清液中sFas含量明显增加(P<0.05);IFN-γ诱导的凋亡率与Fas蛋白表达率的相关性有统计学意义(P<0.05)。结论IFN-γ可以通过调节Fas的表达影响甲状腺细胞凋亡的发生,提示IFN-γ可能通过调节凋亡参与GD的病理生理过程。 Objective To investigate the effects of interferon-γ(IFN-γ) on apoptosis of thyrocytes from patients with Graves disease(GD).Methods Thyrocytes from GD patients were cultured in the absence or presence of IFN-γ at different concentrations.The thyrocyte proliferation was determined by MTT method.Cell apoptosis and Fas expression on thyrocytes were assessed by flow cytometry.The concentration of soluble Fas(sFas) in the culture supernatant was measured by ELISA.Results Compared with the control group(without...
出处 《免疫学杂志》 CAS CSCD 北大核心 2009年第1期88-90,共3页 Immunological Journal
关键词 IFN-γ GRAVES病 甲状腺细胞 细胞凋亡 FAS SFAS IFN-γ Graves disease thyroid apoptosis Fas sFas
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  • 1Novlli F,Giovarelli M,Reber Liske R,et al.Blockade of physiologically secreted IFN-gamma inhibits human T lymphocyte and natural killer cell activation[J].J Immunol,1991,147(4):1 445-1 452.
  • 2Fukushima A,Yamaguchi T,Ishida W,et al.Mice lacking the IFN-gamma receptor or fyn develop severe experimental autoimmune uveoretinitis characterized by different immune responses[J].Immunogenetics,2005,57(5):337-343.
  • 3Vermeire K,Heremans H,Vandeputte M,et al.Accelera-ted collagen-induced arthritis in IFN-gamma receptor-deficient mice[J].J Immunol,1997,158(11):5 507-5 513.
  • 4Zhang GX,Xiao BG,Bai XF,et al.Mice with IFN-gamma receptor deficiency are less susceptible to experimental autoimmune myasthenia gravis[J].J Immunol,1999,162(7):3 775-3 781.
  • 5Alimi E,Huang S,Brazillet MP,et al.Experimental autoimmune thyroiditis (EAT) in mice lacking the IFN-gamma receptor gene[J].Eur J Immunol,1998,28(1):201-208.
  • 6Kaplan C,Valdez JC,Chandrasekaran R,et al.Th1 and Th2 cytokines regulate proteoglycan-specific autoantibody isotypes and arthritis[J].Arthritis Res,2002,4(1):54-58.
  • 7Sakaguchi S,Sakaguchi N,Asano M,et al.Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25).Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases[J].J Immunol,1995,155(3):1 151-1 164.
  • 8Mottet C,Uhlig HH,Powrie F.Cutting edge:cure of colitis by CD4^+CD25^+ regulatory T cells[J].J Immunol,2003,170(8):3 939-3 943.
  • 9Setoguchi R,Hori S,Takahashi T,et al.Homeostatic maintenance of natural Foxp^3+ CD25^+ CD4^+ regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization[J].J Exp Med,2005,201(5):723-735.
  • 10Hori S,Nomura T,Sakaguchi S.Control of regulatory T cell development by the transcription factor Foxp3[J].Science,2003,299(5 609):1 057-1 061.

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