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Arrest chemokines.

Klaus Ley1

  • 1Cardiovascular Research Center and Department of Biomedical Engineering University of Virginia Health System, Charlottesville, VA 22903, USA. klausley@virginia.edu

Microcirculation (New York, N.Y. : 1994)
|July 10, 2003
PubMed
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Arrest chemokines on blood vessel walls capture rolling leukocytes, initiating cell adhesion. While known arrest chemokines exist for lymphocytes and monocytes, none have been identified for neutrophils during inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Vascular Biology

Background:

  • Leukocyte adhesion to endothelium involves capture, rolling, and firm adhesion.
  • Immobilized chemokines binding cognate receptors on rolling cells initiate integrin activation for firm adhesion.
  • Arrest chemokines are crucial for triggering leukocyte arrest on endothelial surfaces.

Purpose of the Study:

  • To review the known arrest chemokines involved in leukocyte adhesion.
  • To highlight the specific arrest chemokines identified for lymphocytes and monocytes.
  • To identify the gap in knowledge regarding arrest chemokines for neutrophils.

Main Methods:

  • Literature review of studies on leukocyte-endothelial interactions.
  • Analysis of chemokines known to immobilize and cause arrest of rolling cells in vitro.

Related Experiment Videos

  • Identification of chemokines demonstrated to function as arrest chemokines under physiologic conditions.

    • Main Results:

    • Secondary lymphoid tissue chemokine (SLC) (CCL21) arrests rolling lymphocytes.
    • Keratinocyte-derived chemokine (KC) (CXCL1), monocyte chemoattractant protein-1 (MCP-1) (CCL2), and RANTES (CCL5) arrest rolling monocytes.
    • No specific arrest chemokines have been identified for neutrophils under inflammatory conditions.

    Conclusions:

    • Arrest chemokines play a vital role in regulating leukocyte trafficking.
    • The known repertoire of physiological arrest chemokines includes SLC, KC, MCP-1, and RANTES.
    • Further research is needed to discover arrest chemokines for neutrophils in inflammatory settings.