CD86 and beta2-adrenergic receptor stimulation regulate B-cell activity cooperatively.

Joseph R Podojil; Virginia M Sanders

doi:10.1016/j.it.2005.02.005

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CD86 and beta2-adrenergic receptor stimulation regulate B-cell activity cooperatively.

Joseph R Podojil·Virginia M Sanders

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Abstract

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.

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Animals Antigens, CD B-Lymphocytes B7-2 Antigen Humans Immunoglobulin G Membrane Glycoproteins Mice Models, Immunological Neuroimmunomodulation Receptors, Adrenergic, beta-2 Signal Transduction Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, P.H.S.Review

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Joseph R Podojil, Virginia M Sanders. 2005. CD86 and beta2-adrenergic receptor stimulation regulate B-cell activity cooperatively.. https://doi.org/10.1016/j.it.2005.02.005

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