Epigallocatechin gallate attenuates adhesion and migration of CD8+ T cells by binding to CD11b
Epigallocatechin gallate attenuates adhesion and migration of CD8+ T cells by binding to CD11b
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DOI：
10.1016/j.jaci.2004.02.044
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发表时间：
2004-06-01
影响因子：
14.2
通讯作者：
Nagawa, H
中科院分区：
文献类型：
--
作者：
Kawai, K;Tsuno, NH;Nagawa, H
背景资料：虽然绿色茶多酚儿茶素已被报道具有抗过敏和抗炎活性，其对免疫系统的影响的确切机制一直缺乏investigated.Objective：在这项研究中，我们的目的是阐明儿茶素的抗炎作用的机制。为此，我们研究了表没食子儿茶素没食子酸酯（epigallocatechin gallate，EGCG）和表儿茶素没食子酸酯（epicatechin gallate）两种儿茶素对免疫应答中起关键作用的外周血CD8（+）T细胞的影响。分离的外周血单核细胞或CD8（+）T细胞在没有或有儿茶素的情况下孵育，流式细胞术检测细胞表面整合素分子表达的变化，竞争性ELISA检测儿茶素与CD11b分子的直接结合。结果：2种儿茶素均能直接与CD8（+）T细胞表面表达的CD11b结合，导致CD11b表达下降。表儿茶素没食子酸酯（epicatechin gallate，EGCG）诱导的CD11b表达受损导致CD8（+）T细胞粘附细胞间粘附分子1的能力降低，从而降低了对趋化因子的迁移反应。我们得出结论，儿茶素，特别是EGCG，通过下调CD8（+）T细胞上的CD11b表达，抑制这些细胞向炎症部位的浸润是一种有前途的新的有效抗炎剂。
Background: Although green tea polyphenol catechin has been reported to have antiallergic and anti-inflammatory activities, the precise mechanisms of its effect on the immune system have been poorly investigated.Objective: In this study, we aimed to elucidate the mechanisms of the anti-inflammatory effect of catechin. For this purpose, we studied the effect of 2 kinds of catechin, epigallocatechin gallate (EGCG) and epicatechin gallate, on peripheral blood CD8(+) T cells, which play the key role in immune responses.Methods: Isolated peripheral blood mononuclear cells or CD8(+) T cells were incubated without or with catechin, and the changes in the surface expression of integrin molecules were investigated by flow cytometry and the direct binding of catechin to CD11b molecule by competitive ELISA. Also, the effect of catechin on the ability of CD8(+) T cells to bind intracellular adhesion molecule 1 and to migrate in response to chemokines was evaluated by using the adhesion and migration assays.Results: The 2 catechins directly bound to CD11b expressed on CD8(+) T cells, which caused a consequent decrease of flow-cytometric CD11b expression. The effect was more prominent with EGCG than epicatechin gallate, and the impaired expression of CD11b induced by EGCG resulted in decreased ability of CD8(+) T cells to adhere intercellular adhesion molecule 1, and consequently decreased migration in response to chemokines.Conclusion: We concluded that catechin, especially EGCG, by downregulating CD11b expression on CD8(+) T cells and, in consequence, inhibiting infiltration of these cells into the sites of inflammation, is a promising new potent anti-inflammatory agent.