期刊
BRAIN BEHAVIOR AND IMMUNITY
卷 17, 期 1, 页码 55-67出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S0889-1591(02)00056-9
关键词
beta-2-adrenergic receptor; norepinephrine; cell-mediated immunity; humoral immunity; adrenergic receptor subtypes; development; homeostasis; in vivo
资金
- NIAID NIH HHS [AI37326, AI47420] Funding Source: Medline
The beta-2-adrenergic receptor (beta(2)AR) is expressed by most lymphocyte populations and binds the sympathetic neurotransmitter norepinephrine (NE). Stimulation of the beta(2)AR 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 beta(2)AR deficient mice (beta(2)AR-/- mice) were all similar to measures made in beta(2)AR+/+ mice. Other members of the adrenergic receptor family did not appear to compensate for the absence in beta(2)AR expression. In contrast, beta(2)AR-/- B cells cultured in vitro were unable to respond to NE in a manner similar to beta(2)AR+/+ B cells. Thus, mice in which expression of the beta(2)AR gene is defective from early development to adulthood may no longer require that NE stimulate the beta(2)AR to maintain immune homeostasis, and this may be due to a non-adrenergic mechanism that provides compensation in vivo. (C) 2002 Elsevier Science (USA). All rights reserved.
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