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Cyclosporine downregulates Fas ligand expression on vascular endothelial cells: implication for accelerated vasculopathy by immunosuppressive therapy.

Abstract：

:Although the introduction of cyclosporine A (CyA) and FK506 for immunosuppressive therapy has dramatically enhanced the early survival of organ transplant recipients, administration of these immunosuppresants is correlated with high incidence of transplant arteriosclerosis. Transplant-associated arteriosclerosis is believed to result from recipient inflammatory responses to the allograft, as it is characterized by early mononuclear cell infiltration of the transplanted vessel. We reported that vascular endothelial cells naturally express a death factor, Fas ligand, that may function to inhibit detrimental leukocyte infiltration. Here, we show that CyA or FK506 downregulates FasL expression on endothelial cells with accompanying decrease in the cytotoxicity toward Fas-bearing cells. Our findings not only demonstrate a novel biological action of these drugs, but also suggest a mechanism by which immunosupressive treatment contributes to atherogenesis.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Sata M,Walsh K

doi

10.1006/bbrc.1999.1392

subject

Has Abstract

pub_date

1999-09-24 00:00:00

pages

430-2

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(99)91392-X

journal_volume

263

pub_type

杂志文章

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