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Differential Usage of Class II Transactivator Promoters PI and PIV during Inflammation and Injury in Kidney

Oki Takeuchi^*, Tasha N. Sims, Yutaka Takei, Vido Ramassar, Konrad S. Famulski and Philip F. Halloran

*Department of Medical Microbiology and Immunology, and Department of Medicine, Division of Nephrology and Immunology, University of Alberta, Edmonton, Alberta, Canada.

Correspondence to Dr. Philip F. Halloran, Division of Nephrology & Immunology, University of Alberta, 250-Heritage Medical Research Centre, Edmonton, Alberta T6G 2S2, Canada. Phone: 780-407-8880; Fax: 780-407-3417;

ABSTRACT. Expression of class II transactivator (CIITA), the transcriptional regulator that controls all class II expression, is controlled in cell lines in vitro by three promoters: the dendritic cell promoter PI, the B cell promoter PIII, and the interferon- (IFN-)–inducible promoter, PIV. The authors examined the promoter usage in vivo in mouse kidney in the basal state and in response to IFN-, endotoxin, allostimulation, and renal injury. Genetically modified mice were used to examine the dependency of each promoter on IFN- and on the transcription factor interferon regulatory factor 1 (IRF-1). Usage of distinct CIITA promoters was monitored by real-time reverse transcriptase polymerase chain reaction (RT-PCR) using the unique sequences in the 5' end of the transcript from each promoter. Kidneys in both control mice and IFN- knockouts expressed chiefly PI- and PIV–related products. Administration of recombinant IFN- activated only promoter PIV. Endotoxin or allogeneic stimulation elevated the PIV-related mRNA, dependent on IFN- and on IRF-1. Ischemic renal injury, however, increased the PI- and PIV–driven mRNA expression in wild-type but also in IFN-–deficient mice. Thus the in vivo control of CIITA promoters in kidney is similar to that observed in vitro (i.e., basal-state usage of PI and IFN-–dependent usage of PIV during inflammation), but it also shows additional levels of control: IFN-–independent basal activity of PIV and IFN-–independent induction of PIV during tissue injury. E-mail: phil.halloran@ualberta.ca

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673