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Protein Kinase C Is Essential to Maintain CIITA Gene Expression in B Cells¹

Myung-Ja Kwon^*, Jae-Won Soh and Cheong-Hee Chang^2,*

^* Department of Microbiology and Immunology, Indiana University School of Medicine and Walther Oncology Center, Indianapolis, IN 46202; and Department of Chemistry, Inha University, Incheon, Korea

Expression of MHC class II genes requires CIITA. Although the transactivation function of CIITA is well characterized, the signaling events that regulate CIITA expression are less understood. In this study, we report that CIITA expression in B cells depends on protein kinase C (PKC). PKC controls CIITA gene transcription mainly via modulating CREB recruitment to the CIITA promoter without affecting CIITA mRNA stability. Inhibition of PKC by a pharmacological inhibitor or knocking down of endogenous PKC expression by small interfering RNA reduced CREB binding to the CIITA promoter. The decrease of CIITA gene expression in the presence of the PKC inhibitor was prevented by ectopically expressing a constitutively active form of CREB. In addition, histone acetylation of the CIITA promoter is regulated by PKC since the PKC inhibitor treatment or PKC small interfering RNA resulted in decreased histone acetylation. Taken together, our study reveals that PKC is an important signaling molecule necessary to maintain CIITA and MHC class II expression in B cells.

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