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首页> 外文期刊>International Journal of Inflammation >Prostaglandin E2Does Not Modulate CCR7 Expression and Functionality after Differentiation of Blood Monocytes into Macrophages
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Prostaglandin E2Does Not Modulate CCR7 Expression and Functionality after Differentiation of Blood Monocytes into Macrophages

机译:血液单核细胞分化为巨噬细胞后,前列腺素E2不会调节CCR7的表达和功能。

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Previously, we demonstrated that prostaglandin E2(PGE2) induces C-C chemokine receptor type 7 (CCR7) expression on human monocytes, which stimulates their subsequent migration in response to the CCR7 natural ligands CCL19 and CCL21. In this study, we determined whether PGE2affects CCR7 expression on macrophages. Flow cytometric analysis and chemotaxis assays were performed on Mono Mac-1-derived macrophage (MDMM-1) as well as unpolarized monocyte-derived macrophages (MDMs) to determine the CCR7 expression and functionality in the presence of PGE2. Data revealed that a MDMM-1 exhibited markedly downregulated CCR7 expression and functionality that were partially restored by treatment with PGE2. In MDMs, we observed a drastic downregulation of CCR7 expression and functionality that were unaffected following PGE2treatment. Our data indicate that monocyte differentiation induces the loss of CCR7 expression and that PGE2is unable to modulate CCR7 expression and functionality as shown previously in monocytes.
机译:以前,我们证明了前列腺素E2(PGE2)诱导人单核细胞上C-C趋化因子受体7型(CCR7)的表达,从而刺激它们随后响应CCR7天然配体CCL19和CCL21迁移。在这项研究中,我们确定PGE2是否影响巨噬细胞上CCR7的表达。流式细胞仪分析和趋化性分析是在Mono Mac-1衍生的巨噬细胞(MDMM-1)以及非极化单核细胞衍生的巨噬细胞(MDM)上进行的,以确定在PGE2存在下CCR7的表达和功能。数据显示,MDMM-1表现出明显下调的CCR7表达和功能,通过PGE2处理可部分恢复。在MDM中,我们观察到CCR7表达和功能的急剧下调在PGE2处理后不受影响。我们的数据表明,单核细胞分化会诱导CCR7表达的丧失,而PGE2无法调节CCR7表达和功能,如先前在单核细胞中所示。

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