Chemokine responsiveness of CD4+ CD25+ regulatory and CD4+ CD25- T cells from atopic and nonatopic donors.
Chemokine responsiveness of CD4+ CD25+ regulatory and CD4+ CD25- T cells from atopic and nonatopic donors.
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DOI：
10.1111/j.1398-9995.2008.01962.x
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发表时间：
2009-08
期刊：
影响因子：
12.4
通讯作者：
Robinson DS
中科院分区：
文献类型：
--
作者：
Ahern D;Lloyd CM;Robinson DS
过敏性炎症与Th2型T细胞相关，其可被CD4+ CD25+调节性T细胞（TcB）抑制。两者都表达趋化因子受体（CCR）4和CCR 8，但表达的动力学和特应性状态的影响尚不清楚。检测来自特应性和非特应性供体的CD4+ CD25+和CD4+ CD25− T细胞的趋化因子受体表达，并记录体外对过敏原刺激的反应。通过流式细胞术和定量PCR检测来自特应性和非特应性的CD4+ CD25 hi和CD4+ CD25− T细胞的趋化因子受体表达。对趋化因子的反应是通过肌动蛋白聚合。通过羧基荧光素琥珀酰亚胺酯标记分析了6天变应原刺激培养物中趋化因子受体表达的动态。CD4+ CD25hi T细胞优先表达CCR3、CCR4、CCR5、CCR6和CCR8。CD4+ CD25hi T细胞对CCR4、CCR6和CCR8的趋化因子配体（分别为CCL17、22、20和1）有应答，在特应性和非特应性供体之间没有差异。在6天的过敏原刺激中，CD4+ CD25+ T细胞下调CCR4并上调CCR7，而CD4+ CD25−效应细胞下调CCR7并上调CCR4。CCR4、CCR6和CCR8在将CD4+ CD25+调节性T细胞和CD4+ CD25−效应性T细胞定位于过敏性炎症部位中具有潜在作用。与效应T细胞的保留相反，过敏原刺激TcR后CCR7的上调和CCR4的下调可能允许它们从炎症部位再循环。
Allergic inflammation is associated with Th2-type T cells, which can be suppressed by CD4+ CD25+ regulatory T cells (Tregs). Both express chemokine receptors (CCR) 4 and CCR8, but the dynamics of expression and effect of atopic status are unknown. To examine the expression of chemokine receptors by CD4+ CD25+ and CD4+ CD25− T cells from atopic and nonatopic donors, and document response to allergen stimulation in vitro. Chemokine receptor expression was examined by flow cytometry and quantitative PCR of CD4+ CD25hi and CD4+ CD25− T cells from atopics and nonatopics. Responsiveness to chemokines was by actin polymerization. Dynamics of chemokine receptor expression in 6-day allergen-stimulated cultures was analysed by carboxyfluoroscein succinimidyl ester labelling. CD4+ CD25hi Tregs preferentially expressed CCR3, CCR4, CCR5, CCR6 and CCR8. CD4+ CD25hi Tregs responded to the chemokine ligands for CCR4, CCR6 and CCR8 (CCL17, 22, 20 and 1 respectively), with no differences between atopic and nonatopic donors. Over 6-day allergen stimulation, CD4+ CD25+ T-cells downregulated CCR4 and upregulated CCR7, in contrast to CD4+ CD25− effector cells, which downregulated CCR7 and upregulated CCR4. CCR4, CCR6 and CCR8 have potential roles in localization of both CD4+ CD25+ regulatory and CD4+ CD25− effector T cells to sites of allergic inflammation. Upregulation of CCR7 and downregulation of CCR4 upon allergen stimulation of Tregs may allow their recirculation from sites of inflammation, in contrast to retention of effector T cells.
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影响因子：
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