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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 beta(2)-adrenergic receptor (beta(2)AR), may cooperate to regulate B cell-associated B7-2 expression in vitro and in vivo. beta(2)AR 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 beta(2)AR stimulation, but not histone hyperacetylation and DNA hypomethylation alone, increased B cell-associated B7-2 expression by increasing B7-2 mRNA stability, NF-kappa B nuclear binding, and NF-kappa B-dependent gene transcription. Thus, this study provides additional insight into the signaling intermediates and molecular mechanisms by which stimulation of the BCR and beta(2)AR may regulate B cell-associated B7-2 expression.

B Cell Receptor- and β2-Adrenergic Receptor-Induced Regulation of B7-2 (CD86) Expression in B Cells