11
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

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

      The Journal of Immunology Author Choice
      Animals, Antigens, CD40, physiology, Cell Communication, Cell Line, Chemokine CCL22, Chemokines, CC, pharmacology, Dendritic Cells, Mice, Mice, Inbred BALB C, Receptors, CCR4, Receptors, Chemokine, T-Lymphocytes

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          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.

          Related collections

          Author and article information

          Comments

          Comment on this article