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Related Experiment Videos

CD40L-CD40 interactions regulate endothelial cell surface tissue factor and thrombomodulin expression

D L Miller1, R Yaron, M J Yellin

  • 1Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

Journal of Leukocyte Biology
|March 21, 1998
PubMed
Summary
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CD40L on T cells directly induces tissue factor and reduces thrombomodulin on endothelial cells, promoting blood clotting during inflammation. This CD40-CD40L interaction is independent of common inflammatory cytokines.

Area of Science:

  • Immunology
  • Vascular Biology
  • Cellular Biology

Background:

  • Activated endothelial cells develop a procoagulant surface during immune responses by altering thrombomodulin and tissue factor expression.
  • CD4+ T cells are known to promote endothelial cell procoagulant activity, but the specific molecular mechanisms remain unclear.

Purpose of the Study:

  • To investigate whether CD40L-CD40 interactions modulate the expression of tissue factor and thrombomodulin on endothelial cells in vitro.
  • To elucidate the role of CD40L expressed on CD4+ T cells in regulating endothelial cell procoagulant function.

Main Methods:

  • Co-culture of human umbilical vein endothelial cells (HUVEC) with Jurkat T cells expressing CD40L.
  • Use of anti-CD40L monoclonal antibody (mAb) to block CD40L-CD40 interactions.

Related Experiment Videos

  • Two-color Fluorescence-Activated Cell Sorting (FACS) analysis to quantify cell surface marker expression.
  • Employing neutralizing antibodies to assess the involvement of specific cytokines (TNF-α, IL-1α, IL-1β).

    • Main Results:

    • CD40 ligation by CD40L directly induces tissue factor expression on HUVEC.
    • CD40 ligation leads to the down-regulation of thrombomodulin on HUVEC.
    • CD40L-mediated modulation of tissue factor and thrombomodulin, along with E-selectin and VCAM-1 upregulation, was independent of TNF-α, IL-1α, or IL-1β.

    Conclusions:

    • CD40L-CD40 interactions directly regulate endothelial cell procoagulant activity.
    • These interactions play a significant role in modulating endothelial cell surface markers during inflammatory responses.
    • The findings suggest a direct pathway for T cell-mediated regulation of vascular hemostasis and inflammation.