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Cutting edge: CCR4 mediates antigen-primed T cell binding to activated dendritic cells.
Wu, M; Fang, H; Hwang, S T.
Affiliation
  • Wu M; Dermatology Branch, National Cancer Institute, Bethesda, MD 20892, USA.
J Immunol ; 167(9): 4791-5, 2001 Nov 01.
Article in En | MEDLINE | ID: mdl-11673480
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.
Subject(s)
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Collection: 01-internacional Database: MEDLINE Main subject: Dendritic Cells / T-Lymphocytes / Receptors, Chemokine Limits: Animals Language: En Journal: J Immunol Year: 2001 Document type: Article Affiliation country: United States
Search on Google
Collection: 01-internacional Database: MEDLINE Main subject: Dendritic Cells / T-Lymphocytes / Receptors, Chemokine Limits: Animals Language: En Journal: J Immunol Year: 2001 Document type: Article Affiliation country: United States