Adaptive immunity in mice lacking the β 2-adrenergic receptor

Abstract

The beta-2-adrenergic receptor (β 2AR) is expressed by most lymphocyte populations and binds the sympathetic neurotransmitter norepinephrine (NE). Stimulation of the β 2AR is reported to be the primary mechanism by which signals from the sympathetic nervous system influence both cell-mediated and humoral immunity. We report here that body/organ weights, lymphoid organ cell number/phenotype/histology, the contact sensitivity response, and the amount, avidity, and isotype of antibody resulting from a T cell-dependent antibody response in β 2AR deficient mice (β 2AR−/− mice) were all similar to measures made in β 2AR+/+ mice. Other members of the adrenergic receptor family did not appear to compensate for the absence in β 2AR expression. In contrast, β 2AR−/− B cells cultured in vitro were unable to respond to NE in a manner similar to β 2AR+/+ B cells. Thus, mice in which expression of the β 2AR gene is defective from early development to adulthood may no longer require that NE stimulate the β 2AR to maintain immune homeostasis, and this may be due to a non-adrenergic mechanism that provides compensation in vivo.