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IL-2和IL-4联合诱导B细胞死亡受体CCR3的表达及其功能研究
CCR3 expression induced by IL-2 and IL-4 as a terminal receptor on germinal center B cells
查看参考文献9篇
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文摘
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目的研究在IL-2和IL-4作用下,趋化性细胞因子受体CCR3在人生发中心(germinal center,GC)B细胞上的表达及其功能特性.方法采用流式细胞术检测人GC B细胞上CCR3表达和在CCR3配体eotaxin作用下B细胞的凋亡,实时定量RT-PCR和Northern blot法检测GC B细胞内CCR3 mRNA的表达,淋巴细胞趋化和黏附试验检测B细胞的趋化和黏附能力.结果人GC B细胞极低表达趋化性细胞因子受体CCR3,经IL-2和IL-4作用后,GC B细胞高表达CCR3,但此时CCR3不能在其配体作用下诱导GC B细胞的趋化和黏附功能,而是诱导GC B细胞凋亡.结论IL-2和IL-4联合诱导人GC B细胞CCR3表达,CCR3可能具有死亡受体的功能. |
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其他语种文摘
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Objective To study the expression and functions of chemokine receptor CCR3 induced by the action of 11-2 and IL-4 on human germinal center (GC) B cells. Methods Plow cytometry was used to detect the expression of CCR3 in GC B cells as well as the apoptosis of GC B cells. Realtime quantitative reverse tran-scription (RT)-PCR and Northern blot assay were utilized to analyze the CCR3 mRNA expressed in the GC B cells. Chemotaxis and adhesion assay were exploited to determine GC B cell chemotaxis and adhesion induced by CCR3 and its ligand. Results There was few CCR3 expressed in human GC B cells. Combination of IL-2 and IL-4 were able to up-regulated CCR3 molecule expression in GC B cells as well as CCR3 mRNA in the cells. Eotaxin, the ligand to CCR3, could not induce GC B cell chenaotaxis and adhesion. However, it triggered apoptosjs of GC B cells. Conclu-sion Combination of IL-2 and IL-4 can induce expression of CCR3, which acts as a death receptor on GC B cells. |
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来源
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中华微生物学和免疫学杂志
,2004,24(7):505-508 【核心库】
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关键词
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趋化性细胞因子受体
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生发中心B细胞
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凋亡
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IL-2
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IL-4
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地址
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武汉大学医学院免疫系, 430071
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语种
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中文 |
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文献类型
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研究性论文 |
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ISSN
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0254-5101 |
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学科
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基础医学 |
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文献收藏号
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CSCD:1660750
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参考文献 共
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