Adaptive immunity in mice lacking the β2-adrenergic receptor

Virginia M. Sanders*, Deborah J. Kasprowicz, Michelle A. Swanson-Mungerson, Joseph R. Podojil, Adam P. Kohm

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


The beta-2-adrenergic receptor (β2AR) is expressed by most lymphocyte populations and binds the sympathetic neurotransmitter norepinephrine (NE). Stimulation of the β2AR 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 β2AR deficient mice (β2AR-/- mice) were all similar to measures made in β2AR+/+ mice. Other members of the adrenergic receptor family did not appear to compensate for the absence in β2AR expression. In contrast, β2AR-/- B cells cultured in vitro were unable to respond to NE in a manner similar to β2AR+/+ B cells. Thus, mice in which expression of the β2AR gene is defective from early development to adulthood may no longer require that NE stimulate the β2AR to maintain immune homeostasis, and this may be due to a non-adrenergic mechanism that provides compensation in vivo.

Original languageEnglish (US)
Pages (from-to)55-67
Number of pages13
JournalBrain, Behavior, and Immunity
Issue number1
StatePublished - Feb 2003


  • Adrenergic receptor subtypes
  • Beta-2-adrenergic receptor
  • Cell-mediated immunity
  • Development
  • Homeostasis
  • Humoral immunity
  • In vivo
  • Norepinephrine

ASJC Scopus subject areas

  • Endocrine and Autonomic Systems
  • Behavioral Neuroscience
  • Immunology


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