CD86 and β2-adrenergic receptor stimulation regulate B-cell activity cooperatively

IgG1 functions to neutralize and clear foreign antigens, such as extracellular bacteria. Therefore, it is important to understand the multiple mechanisms by which the level of IgG1 is regulated to maintain immune system and host homeostasis. Recent data show that the level of IgG1 produced by a B cell is increased following CD86 and β2-adrenergic receptor (β2AR) stimulation, through increased expression of the transcription factor Oct-2 and its coactivator OCA-B (Oct coactivator from B cells), respectively. This finding suggests that signaling pathways that are activated by an immunoreceptor (CD86) and a neuroreceptor (β2AR) converge to regulate the IgG1 response.