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CC趋化因子受体CCR-1和CCR-3可能参与人外周血单核细胞源性树突状细胞的抗原呈递细胞功能。

CC chemokine receptors, CCR-1 and CCR-3, are potentially involved in antigen-presenting cell function of human peripheral blood monocyte-derived dendritic cells.

作者信息

Sato K, Kawasaki H, Nagayama H, Serizawa R, Ikeda J, Morimoto C, Yasunaga K, Yamaji N, Tadokoro K, Juji T, Takahashi T A

机构信息

Department of Cell Processing, Department of Clinical Immunology and AIDS Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

出版信息

Blood. 1999 Jan 1;93(1):34-42.

PMID:9864143
Abstract

We examined the potential involvement of two CC chemokine receptors (CCRs), CCR-1 and CCR-3, in the functional activation of granulocyte-macrophage colony-stimulating factor (GM-CSF) plus interleukin-4 (IL-4)-generated human peripheral blood monocyte-derived immature dendritic cells (DCs). Flow cytometric analysis showed that CCR-1, CCR-3, CCR-5, and CXC chemokine receptor (CXCR)-4 were expressed on the cell surface of monocyte-derived DCs. Treatment with a monoclonal antibody (MoAb) to either CCR-1 or CCR-3 but not MoAbs to CCR-5 and CXCR-4 abolished chemotactic migration of monocyte-derived DCs. The DCs treated with either the anti-CCR-1 MoAb or anti-CCR-3 MoAb were less efficient than untreated DCs in proliferation of allogeneic T cells (TCs) and TC-derived secretion of interferon-gamma (IFN-gamma). The homotypic aggregation of DCs and heterotypic aggregation of DCs with TCs were suppressed by the anti-CCR-1 MoAb or anti-CCR-3 MoAb. These results indicate that CCR-1 and CCR-3 specifically regulate interaction of TCs and DCs in the process of antigen presentation.

摘要

我们研究了两种CC趋化因子受体(CCR),即CCR-1和CCR-3,在粒细胞-巨噬细胞集落刺激因子(GM-CSF)加白细胞介素-4(IL-4)诱导产生的人外周血单核细胞来源的未成熟树突状细胞(DC)功能激活中的潜在作用。流式细胞术分析显示,CCR-1、CCR-3、CCR-5和CXC趋化因子受体(CXCR)-4在单核细胞来源的DC细胞表面表达。用针对CCR-1或CCR-3的单克隆抗体(MoAb)处理单核细胞来源的DC可消除其趋化迁移,而用针对CCR-5和CXCR-4的MoAb处理则无此作用。用抗CCR-1 MoAb或抗CCR-3 MoAb处理的DC在同种异体T细胞(TC)增殖及TC分泌干扰素-γ(IFN-γ)方面的效率低于未处理的DC。抗CCR-1 MoAb或抗CCR-3 MoAb可抑制DC的同型聚集以及DC与TC的异型聚集。这些结果表明,CCR-1和CCR-3在抗原呈递过程中特异性调节TC与DC的相互作用。

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