CD86 and beta2-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 beta2-adrenergic receptor (beta2AR) 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 (beta2AR) converge to regulate the IgG1 response.
Podojil
Joseph R
JR
Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, OH 43210, USA.
Sanders
Virginia M
VM
D000818:Animals; D015703:Antigens, CD / Q000378:metabolism*; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism*; D051940:B7-2 Antigen; D006801:Humans; D007074:Immunoglobulin G / Q000096:biosynthesis; D008562:Membrane Glycoproteins / Q000378:metabolism*; D051379:Mice; D018448:Models, Immunological; D015213:Neuroimmunomodulation; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism*; D015398:Signal Transduction
D015703:Antigens, CD; D051940:B7-2 Antigen; C497964:CD86 protein, human; C497965:Cd86 protein, mouse; D007074:Immunoglobulin G; D008562:Membrane Glycoproteins; D018343:Receptors, Adrenergic, beta-2