Open AccessCD40 on human endothelial cells: inducibility by cytokines and functional regulation of adhesion molecule expression.
Author(s) -
Karin Karmann,
Christopher C.W. Hughes,
Jeffrey S. Schechner,
William C. Fanslow,
Jordan S. Pober
Publication year - 1995
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.92.10.4342
Subject(s) - cd40 , cell adhesion molecule , tumor necrosis factor alpha , cytokine , intercellular adhesion molecule 1 , e selectin , biology , umbilical vein , microbiology and biotechnology , cell adhesion , intercellular adhesion molecule , monoclonal antibody , interferon gamma , endothelial stem cell , immunology , antibody , cell , biochemistry , in vitro , cytotoxic t cell
Cultured human umbilical vein endothelial cells (EC) constitutively express a low level of CD40 antigen as detected by monoclonal antibody binding and fluorescence flow cytometric quantitation. The level of expression on EC is increased about 3-fold following 24 h treatment with optimal concentrations of tumor necrosis factor, interleukin 1, interferon beta, or interferon gamma; both interferons show greater than additive induction of CD40 when combined with tumor necrosis factor or interleukin 1. Expression of CD40 increases within 8 h of cytokine treatment and continues to increase through 72 h. A trimeric form of recombinant murine CD40 ligand acts on human EC to increase expression of leukocyte adhesion molecules, including E-selectin, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1. CD40 may be detected immunocytochemically on human microvascular EC in normal skin. We conclude that endothelial CD40 may play a role as a signaling receptor in the development of T-cell-mediated inflammatory reactions.