Wu, J and Ma, H and Fan, ST and Schlitt, HJ and Tsui, TY (2005) Bilirubin derived from heme degradation suppresses MHC class II expression in endothelial cells. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 338 (2). pp. 890-896. ISSN 0006-291X, 1090-2104
Full text not available from this repository. (Request a copy)Abstract
The enzymatic action of heme oxygenase (HO) is mediated by the cleavage of heme into carbon monoxide, ferrous iron, and biliverdin/bilirubin. Here, we show that induction of HO-1 expression, an inducible form of HO, down-regulmes IFN-gamma-induced MHC class II expression in endothelial cells. Among three catalytic products of HO, bilirubin, but not carbon monoxide or ferrous iron, mediated the suppressive effects of HO through the reduction of mRNA levels of Stat-1-dependent class II transactivator. Expression of HO-1 could suppress the levels of IFN-gamma-induced Stat-1 phosphorylation. This effect could be mimicked by exposing the cells to one of its catalytic products, bilirubin. In addition, HO-I or bilirubin could modulate the transcript activities of Stat-1-driven gene expression in luciferase reporter assays. These findings suggest an important role of HO-1 in the modulation of immune responses through suppression of MHC-II expression in antigen presenting cells. Our data provide a new line of evidence supporting HO-1-targeted therapy for immune modulation. (c) 2005 Elsevier Inc. All rights reserved.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | CARBON-MONOXIDE; OXYGENASE-1; GENE; INJURY; MICE; LIPOPOLYSACCHARIDE; INTERLEUKIN-10; REJECTION; HEARTS; bilirubin; major histocompatibility complex class II; heme oxygenase-1; endothelial cells; interferon-gamma |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Chirurgie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 04 Mar 2021 10:05 |
| Last Modified: | 04 Mar 2021 10:05 |
| URI: | https://pred.uni-regensburg.de/id/eprint/35313 |
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