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Originally published In Press as doi:10.1074/jbc.M101295200 on March 13, 2001

J. Biol. Chem., Vol. 276, Issue 22, 19089-19093, June 1, 2001
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Dendritic Cell-specific MHC Class II Transactivator Contains a Caspase Recruitment Domain That Confers Potent Transactivation Activity*

Kevin NickersonDagger §, Tyler J. SiskDagger §, Naohiro Inohara§, Christina S. K. YeeDagger , Jennifer Kennell||, Min-Chul Cho**, P. Joseph Yannie IIDagger Dagger , Gabriel Núñez, and Cheong-Hee ChangDagger §§

From the Departments of Dagger  Microbiology and Immunology,  Pathology and Comprehensive Cancer Center, || Cellular and Molecular Biology, ** Biology, and Dagger Dagger  Surgery, University of Michigan Medical School, Ann Arbor, Michigan 48109

The MHC class II transactivator (CIITA) is a critical transcription factor that regulates genes involved in antigen presentation function. At least three functional forms of CIITA gene products are transcribed from three different promoters. The CIITA gene expressed in dendritic cells (DC-CIITA) has a unique first exon encoding an extended N-terminal region of CIITA. Here, we show that the N terminus of DC-CIITA has high homology to a caspase recruitment domain (CARD) found in components of apoptosis and nuclear factor-kappa B signaling pathways. However, DC-CIITA does not regulate cell death, nor does it induce nuclear factor-kappa B activity. Instead, DC-CIITA is transcriptionally a more potent activator of the MHC class II gene than the form expressed in B cells. A single amino acid substitution in the CARD of DC-CIITA, predicted to disrupt CARD-CARD interactions, diminished the transactivation potential of DC-CIITA. These results indicate that the CARD in the context of CIITA serves as a regulatory domain for transcriptional activity and may function to selectively enhance MHC class II gene expression in dendritic cells.

* This work was supported by National Institutes of Health Grant AI41510 (to C. -H. C.), National Institutes of Health Immunology Training Grant T32-AI07413 (to T.  S.), National Institutes of Health National Research Service Award 5-T32-GM07544 from the National Institutes of General Medicine Sciences (to K. N.), and the National Institutes of Health Medical Scientist Training Program Student Training Grant T32-GM07863 (to C. S. K. Y.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ These authors contributed equally to this work.

§§ To whom correspondence should be addressed: Dept. of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109. Tel.: 734-647-7666; Fax: 734-764-3562; E-mail: heechang@umich.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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