Selective aryl hydrocarbon receptor modulator-mediated repression of CD55 expression induced by cytokine exposure.

The Journal of Pharmacology and Experimental Therapeutics
Gitanjali A NarayananGary H Perdew

Abstract

Modulation of aryl hydrocarbon receptor (AHR) activity by a class of ligands termed selective AHR modulators (SAhRMs) has been demonstrated to attenuate proinflammatory gene expression and signaling, including repression of cytokine-mediated induction of acute-phase genes (e.g., Saa1). These effects are observed to occur through an AHR-dependent mechanism that does not require canonical signaling through dioxin response elements. Previously, we have demonstrated that the SAhRM 3',4'-dimethoxy-α-naphthoflavone (DiMNF) can repress the cytokine-mediated induction of complement factor genes. Here, we report that the activation of the AHR with DiMNF can suppress cytokine-mediated induction of the membrane complement regulatory protein CD55. When CD55 is expressed on host cells, it facilitates the decay of the complement component 3 (C3) convertase, thereby protecting the cell from complement-mediated lysis. Tumor cells often exhibit elevated CD55 expression on the cell surface in the inflammatory microenvironment of the tumor, and such enhanced expression could represent a means of escaping immune surveillance. DiMNF can repress the cytokine-mediated induction of CD55 mRNA and protein. Luciferase reporter analysis has identified pos...Continue Reading

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Citations

Apr 3, 2013·Journal of Molecular Histology·Ziyu LiuZhikai Xu
Apr 11, 2014·Toxicological Sciences : an Official Journal of the Society of Toxicology·Gregory D KennedyChristopher A Bradfield
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Aug 16, 2017·Experimental and Therapeutic Medicine·Wenqiang LiYingguang Xie
Mar 11, 2018·Joint, Bone, Spine : Revue Du Rhumatisme·Johanna SigauxMarie-Christophe Boissier

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