Cutting edge: CCR4 mediates antigen-primed T cell binding to activated dendritic cells

被引:40
作者
Wu, MT [1 ]
Fang, H [1 ]
Hwang, ST [1 ]
机构
[1] NCI, Dermatol Branch, Bethesda, MD 20892 USA
关键词
D O I
10.4049/jimmunol.167.9.4791
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The binding of a T cell to an Ag-laden dendritic cell (DC) is a critical step of the acquired immune response. Herein, we address whether a DC-produced chemokine can induce the arrest of T cells on DC under dynamic flow conditions. Ag-primed T cells and a T cell line were observed to rapidly (similar to0.5 s) bind to immobilized DC at low shear stress (0.1-0.2 dynes/cm(2)) in a pertussis toxin-sensitive fashion. Quantitatively, Ag-primed T cells displayed 2- to 3-fold enhanced binding to DC compared with unprimed T cells (p < 0.01). In contrast to naive T cells, primed T cell arrest was largely inhibited by pertussis toxin, neutralization of the CC chemokine, macrophage-derived chemokine (CCL22), or by desensitization of the CCL22 receptor, CCR4. Our results demonstrate that DC-derived CCL22 induces rapid binding of activated T cells under dynamic conditions and that Ag-primed and naive T cells fundamentally differ with respect. to chemokine-dependent binding to DC.
引用
收藏
页码:4791 / 4795
页数:5
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