Abstract

Endogenous physiological mechanisms are in place to regulate cell activity in organ systems to maintain host homeostasis when challenged. Antigenic exposure is an example of a challenge that disrupts host homeostasis. During this challenge, activated immune cells secrete cytokines that influence central nervous system activity, which in turn activates the peripheral sympathetic nervous system to release the neurotransmitter norepinephrine from nerve terminals located within lymphoid tissues. Norepinephrine binds to the beta2-adrenergic receptor expressed on immune cells to regulate the level of gene expression and the magnitude of an immune response. In this review, we will discuss both in vitro and in vivo findings that indicate the cellular and molecular mechanisms by which norepinephrine stimulation of the beta2- adrenergic receptor on CD4+ T cells and B cells regulates the level of cellular activity to maintain host homeostasis.

Keywords: Sympathetic nervous system, norepinephrine, CD4+ T cell, B cell, antibody