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Updated: Aug 10, 2026
14:16
Analysis of Physiologic E-Selectin-Mediated Leukocyte Rolling on Microvascular Endothelium
Published on: February 11, 2009
Tumor necrosis factor-induced E-selectin expression on vascular endothelial cells
1Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee 53201-1997, USA.
Critical Care Medicine
|September 1, 1996
Summary
Tumor necrosis factor (TNF) activates E-selectin expression on endothelial cells via both CD120a and CD120b receptors. Blocking these TNF receptors can inhibit E-selectin expression, with synergistic effects when both are blocked.
Area of Science:
- Immunology
- Cell Biology
- Vascular Biology
Background:
- Tumor necrosis factor (TNF) plays a crucial role in inflammatory responses.
- E-selectin is an adhesion molecule expressed on endothelial cells during inflammation.
- The specific TNF receptors mediating E-selectin induction require elucidation.
Purpose of the Study:
- To identify the specific tumor necrosis factor (TNF) receptor subtypes responsible for inducing E-selectin expression on vascular endothelial cells.
- To investigate the role of CD120a and CD120b receptors in TNF-mediated E-selectin upregulation.
Main Methods:
- In vitro study using cultured human umbilical vein endothelial cells.
- Recombinant human TNF (rhTNF) was used to induce E-selectin expression.
- Monoclonal antibodies against TNF receptors (anti-CD120a and anti-CD120b) were employed to block receptor binding.
- E-selectin expression was quantified using indirect immunofluorescence and flow cytometry.
Main Results:
- Blocking either CD120a or CD120b receptors individually significantly inhibited TNF-induced E-selectin expression.
- Simultaneous blockade of both CD120a and CD120b receptors resulted in synergistic inhibition.
- The degree of E-selectin expression inhibition was dependent on both TNF and antibody concentrations.
Conclusions:
- Both CD120a and CD120b receptors are critically involved in TNF-induced E-selectin expression on human umbilical vein endothelial cells.
- Targeting either or both TNF receptors can modulate E-selectin expression, offering potential therapeutic strategies.
- The inhibitory effect on E-selectin expression is concentration-dependent on both TNF and blocking antibodies.
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