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J. Biol. Chem., Vol. 279, Issue 22, 23394-23404, May 28, 2004

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CD86 and ₂-Adrenergic Receptor Signaling Pathways, Respectively, Increase Oct-2 and OCA-B Expression and Binding to the 3'-IgH Enhancer in B Cells^*

Joseph R. Podojil, Nicholas W. Kin, and Virginia M. Sanders¶

From the Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, Ohio 43210

Stimulation of CD86 (formerly known as B7-2) and/or the ₂-adrenergic receptor on a CD40 ligand/interleukin-4-activated B cell increased the rate of mature IgG₁ transcription. To identify the mechanism responsible for this effect, we determined whether CD86 and/or ₂-adrenergic receptor stimulation regulated transcription factor expression and binding to the 3'-IgH enhancer in vitro and in vivo. We showed that CD86 stimulation increased the nuclear localization of NF-B1 (p50) and phosphorylated RelA (p65) and increased Oct-2 expression and binding to the 3'-IgH enhancer, in a protein kinase C-dependent manner. These effects were lost when CD86-deficient or NF-B1-deficient B cells were used. CD86 stimulation also increased the level of IB- phosphorylation but in a protein kinase C-independent manner. ₂-Adrenergic receptor stimulation increased CREB phosphorylation, OCA-B expression, and OCA-B binding to the 3'-IgH enhancer in a protein kinase A-dependent manner, an effect lost when ₂-adrenergic receptor-deficient B cells were used. Also, the ₂-adrenergic receptor-induced increase in the level of mature IgG₁ transcript was lost when OCA-B-deficient B cells were used. These data are the first to show that CD86 stimulation up-regulates the expression of the transcription factor Oct-2 in a protein kinase C- and NF-B1-dependent manner, and that ₂-adrenergic receptor stimulation up-regulates the expression of the coactivator OCA-B in a protein kinase A-dependent manner to cooperate with Oct-2 binding to the 3'-IgH enhancer.

Received for publication, December 1, 2003 , and in revised form, February 17, 2004.

^* This work was supported in part by National Institutes of Health Grants AI37326 and AI47420. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Performed this work as part of the dissertation research as predoctoral student in the Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL 60153.

Recipient of National Institutes of Health Training Grant T32 AI55411.

^¶ To whom correspondence should be addressed: Dept. of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, 2194 Graves Hall, 333 West 10th St., Columbus, OH 43210. Tel.: 614-292-3349; Fax: 614-292-9805; E-mail: Sanders.302{at}osu.edu.

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