CCR4和CCR10在表皮角质形成细胞上表达，并参与皮肤免疫反应。

CCR4 and CCR10 are expressed on epidermal keratinocytes and are involved in cutaneous immune reaction.

作者信息

Fujimoto Seiki, Uratsuji Hideya, Saeki Hidehisa, Kagami Shinji, Tsunemi Yuichiro, Komine Mayumi, Tamaki Kunihiko

机构信息

Department of Dermatology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.

出版信息

Cytokine. 2008 Oct;44(1):172-8. doi: 10.1016/j.cyto.2008.07.472. Epub 2008 Sep 7.

DOI:10.1016/j.cyto.2008.07.472

PMID:18782672

Abstract

CC chemokine ligand (CCL)17 and CCL27 produced by epidermal keratinocytes (KCs) recruit CC chemokine receptor (CCR)4 and CCR10 expressing T cells into the skin, respectively, resulting in enhanced skin inflammation. However, CCR4/CCL17 and CCR10/CCL27 interactions in epidermal KCs have not been investigated. The purpose of this study was to evaluate the role of the CCR4/CCL17 and CCR10/CCL27 loops in cutaneous immune reaction. Normal human KCs (NHKs) and HaCaT KCs expressed both CCR4 and CCR10 at mRNA and protein levels. CCR4 ligand CCL17 but not CCR10 ligand CCL27 induced production of IL-12 p40, granulocyte/monocyte colony-stimulating factor (GM-CSF) and nerve growth factor (NGF) by KCs. Both CCL17 and CCL27 induced migration of KCs in Boyden chamber assay and wound scratch assay. This study revealed that CCR4 and CCR10 are expressed on epidermal KCs and that both are functional in terms of skin cytokine production and/or migration to their ligand CCL17 and CCL27, respectively. Thus this study provided new insight into chemokine/chemokine receptors of KCs.

摘要

由表皮角质形成细胞（KC）产生的CC趋化因子配体（CCL）17和CCL27分别将表达CC趋化因子受体（CCR）4和CCR10的T细胞募集到皮肤中，从而导致皮肤炎症加剧。然而，表皮KC中CCR4/CCL17和CCR10/CCL27的相互作用尚未得到研究。本研究的目的是评估CCR4/CCL17和CCR10/CCL27环路在皮肤免疫反应中的作用。正常人KC（NHK）和HaCaT KC在mRNA和蛋白质水平均表达CCR4和CCR10。CCR4配体CCL17而非CCR10配体CCL27可诱导KC产生白细胞介素-12 p40、粒细胞/单核细胞集落刺激因子（GM-CSF）和神经生长因子（NGF）。在Boyden小室试验和伤口划痕试验中，CCL17和CCL27均可诱导KC迁移。本研究表明，CCR4和CCR10在表皮KC上表达，并且二者分别在皮肤细胞因子产生和/或向其配体CCL17和CCL27迁移方面发挥作用。因此，本研究为KC的趋化因子/趋化因子受体提供了新的见解。