Cutting edge: CCR4 mediates antigen-primed T cell binding to activated dendritic cells. |
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Authors: | M Wu H Fang S T Hwang |
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Affiliation: | Dermatology Branch, National Cancer Institute, Bethesda, MD 20892, USA. |
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Abstract: | 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 ( approximately 0.5 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. |
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