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Related Experiment Videos

Chemokines have diverse abilities to form solid phase gradients.

D D Patel1, W Koopmann, T Imai

  • 1Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA. patel003@mc.duke.edu

Clinical Immunology (Orlando, Fla.)
|April 5, 2001
PubMed
Summary

Chemokines can bind to extracellular matrix and mast cells in rheumatoid arthritis synovium via glycosaminoglycans. Only some chemokines efficiently bind, suggesting complex extravascular chemotactic gradients.

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Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Chemokines are crucial for leukocyte recruitment in inflammatory conditions like rheumatoid arthritis (RA).
  • While immobilized chemokines on endothelium promote leukocyte adhesion, the role of extravascular chemokines in leukocyte extravasation is less understood.
  • Understanding chemokine immobilization in the tissue microenvironment is key to deciphering leukocyte migration dynamics.

Purpose of the Study:

  • To investigate if chemokines can immobilize onto structures within the extravascular space.
  • To elucidate the mechanisms underlying chemokine immobilization in situ.
  • To assess the differential potential of various chemokines to form solid-phase gradients.

Main Methods:

  • Utilized secreted alkaline phosphatase (SEAP)-tagged chemokines and fusion proteins to assess binding to mast cells and extracellular matrix (ECM) in RA synovium.

Related Experiment Videos

  • Investigated the role of salt concentration and glycosaminoglycans (GAGs) in chemokine binding.
  • Correlated chemokine binding avidity to heparin with their ability to bind to synovial structures.
  • Assessed a RANTES mutant with reduced heparin-binding avidity.

    • Main Results:

    • SEAP-tagged chemokines SLC, TARC, and RANTES bound to mast cells and ECM in RA synovium, unlike MCP1, MIP1 alpha, MIP1 beta, and fractalkine.
    • Chemokine binding was inhibited by high salt and sulfated GAGs (heparin, heparan sulfate, chondroitin sulfate, dermatan sulfate), but not dextran or hyaluronan.
    • Binding affinity to synovial structures correlated with heparin-binding avidity, and a RANTES mutant showed impaired binding.
    • A subset of chemokines demonstrated efficient binding to extravascular structures.

    Conclusions:

    • Chemokines can immobilize onto ECM and mast cell components in the RA synovium through interactions with highly sulfated GAGs.
    • The ability of chemokines to bind to extravascular structures varies significantly, influencing the formation of chemotactic gradients.
    • These findings suggest that extravascular chemokine gradients are complex and depend on the specific chemokine's GAG-binding properties.