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B Cell Receptor- and ₂-Adrenergic Receptor-Induced Regulation of B7-2 (CD86) Expression in B Cells¹

Adam P. Kohm^2,*, Afsaneh Mozaffarian^3,* and Virginia M. Sanders^4,*,

^* Departments of Cell Biology, Neurobiology, and Anatomy, and Microbiology and Immunology, Loyola University Stritch School of Medicine, Maywood, IL 60153

The costimulatory molecule B7-2 (CD86) is expressed on the surface of APCs, including B cells. Considering the importance of B7-2 in regulating both T and B cell function, it may be important to understand the regulatory mechanisms governing its expression. We report in this study that stimulation of the B cell receptor (BCR) and/or a neurotransmitter receptor, the ₂-adrenergic receptor (₂AR), may cooperate to regulate B cell-associated B7-2 expression in vitro and in vivo. ₂AR stimulation further enhanced the level of BCR-induced B7-2 expression in B cells potentially via protein tyrosine kinase-, protein kinase A-, protein kinase C-, and mitogen-activated protein kinase-dependent mechanisms. Importantly, BCR and/or ₂AR stimulation, but not histone hyperacetylation and DNA hypomethylation alone, increased B cell-associated B7-2 expression by increasing B7-2 mRNA stability, NF-B nuclear binding, and NF-B-dependent gene transcription. Thus, this study provides additional insight into the signaling intermediates and molecular mechanisms by which stimulation of the BCR and ₂AR may regulate B cell-associated B7-2 expression.

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