Abstract
Study Objective: This project sought to elucidate the biological mechanisms and physiological significance of β2 adrenergic receptor (B2AR)- and M1 muscarinic receptor (M1R)-mediated modulation of NF-κB signaling through the β-arrestins. Differential regulation of immune and inflammatory responses by the sympathetic and parasympathetic nervous system has been previously described. Adrenergic receptors and muscarinic receptors, both expressed on leukocytes, suppress and activate, respectively, humoral and cell-mediated immune responses; however, the mechanisms underlying these responses is unknown. Furthermore, the multifunctional scaffolding proteins β-arrestin 1 and β-arrestin 2 have been implicated in regulation of both pro-
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