Tumor Necrosis Factor c ~ ( TNF - c ~ ) - induced Cell Adhesion to Human Endothelial Cells Is under Dominant Control of One TNT Receptor Type

نویسندگان

  • Fabienne Mackay
  • Hansruedi Loetscher
  • Dietrich Stueber
  • Gisela Gehr
  • Werner Lesslauer
چکیده

Tumor necrosis factor ot (TNF-ot) is a pleiotropic cytokine triggering cell responses through two distinct membrane receptors. Stimulation of leukocyte adhesion to the endothelium is one of the many TNF-ot activities and is explained by the upregulation of adhesion molecules on the endothelial cell surface. Human umbilical vein endothelial cells (HUVEC) were isolated, cultured, and demonstrated to express both TNF receptor types, TNF-K55 and TNF-R75. Cell adhesion to HUVEC was studied using the HL60, U937, and MOLT-4 cell lines. HUVEC were activated by either TNF-ot, binding to both TNF-R55 and TNF-K75, and by receptor type-specific agonists, binding exclusively to TNF-R55 or to TNF-K75. The TNF-ot-induced cell adhesion to HUVEC was found to be controlled almost exclusively by TNF-R55. This finding correlated with the exclusive activity of TNF-K55 in the TNF-ot-dependent regulation of the expression of the intercellular adhesion molecule type 1 (ICAM-1), E-selectin, and vascular cell adhesion molecule type 1 (VCAM-1). The CD44 adhesion molecule in HUVEC was also found to be upregulated through TNF-K55. However, both TNF-R55 and TNF-R75 upregulate ot2 integrin expression in HUVEC. The predominant role of TNF-R55 in TNF-ot-induced adhesion in HUVEC may correlate with its specific control of NF-xB activation, since xB elements are known to be present in ICAM-1, E-selectin, and VCAM-1 gene regulatory sequences.

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تاریخ انتشار 2003