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Related Experiment Videos

Human allogeneic lymphocytes trigger endothelial cell tissue factor expression by a tumor necrosis factor-dependent

P Reverdiau-Moalic1, H Watier, S Iochmann

  • 1Laboratoire d'Hémostase foetale, UPRES-JE 1992 Interactions Hôte-Greffon, Faculté de Médecine de Tours.

The Journal of Laboratory and Clinical Medicine
|December 16, 1998
PubMed
Summary

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Lymphocytes induce tissue factor (TF) expression in endothelial cells, promoting blood clotting during allograft rejection. This process requires cell contact and involves tumor necrosis factor-alpha (TNF-alpha) signaling pathways.

Area of Science:

  • Immunology
  • Vascular Biology
  • Coagulation Science

Background:

  • Lymphocyte adhesion and fibrin deposition are key in allograft rejection.
  • Endothelial cells play a crucial role in regulating coagulation.
  • Understanding endothelial cell activation is vital for managing immune responses.

Purpose of the Study:

  • To investigate the induction of tissue factor (TF) expression on human umbilical vein endothelial cells (HUVECs) by allogeneic lymphocytes (PBLs).
  • To elucidate the signaling pathways involved in PBL-induced TF expression.
  • To assess the role of TF in the context of allograft rejection.

Main Methods:

  • Co-culture of HUVECs with PBLs.
  • Factor Xa generation assay to measure TF activity.

Related Experiment Videos

  • Reverse transcription-polymerase chain reaction (RT-PCR) for TF mRNA detection.
  • Inhibition studies using cycloheximide and actinomycin D.
  • Analysis of TNF-alpha receptor interactions and downstream signaling molecules.

    • Main Results:

    • HUVECs expressed significant procoagulant activity via the TF/factor VII pathway upon co-culture with PBLs.
    • TF activity was enhanced by interferon-gamma (IFN-gamma) and required direct cell-cell contact.
    • PBL-induced TF expression involved de novo protein synthesis, confirmed by increased TF mRNA.
    • Signaling pathways included membrane TNF-TNFR interaction, platelet-activating factor, P-selectin, protein kinase C, and protein tyrosine kinases.

    Conclusions:

    • PBLs induce TF expression in HUVECs through a contact-dependent mechanism involving TNF-alpha signaling.
    • This TF induction contributes to the procoagulant state relevant to allograft rejection.
    • The findings highlight a critical interplay between immune cells and the coagulation system in pathological conditions.