Β-Arrestin 2-Mediated Immune Suppression Induced by Chronic Stress
Document Type
Article
Publication Date
3-1-2011
Description
Objective: Stress, either physical or psychological, can modulate immune function. However, the mechanisms associated with stress-induced immune suppression remain to be elucidated. β-Arrestin 2 serves as adaptor, scaffold, and/or signal transducer. The role of β-arrestin 2 in stress-induced immune suppression is not known yet. Methods/Results: Here, we demonstrate that β-arrestin 2 deficiency in mice increases the sensitivity to the chronic stress-induced reduction in the number of splenocytes. Interestingly, the stress-induced suppression of T helper-type (Th) 1 cytokines and the increased production of Th2 cytokines were greatly enhanced in β-arrestin 2-deficient mice compared with wild-type mice. Moreover, inhibition of PI3K in β-arrestin 2-deficient mice exerts an additive effect on the stress-induced reduction in the number of splenocytes. Conclusion: Our study demonstrates that a deficiency in β-arrestin 2 augments stress-induced immune suppression.
Citation Information
Li, Hui; Smalligan, Dean A.; Xie, Nanchang; Javer, Avani; Zhang, Yi; Hanley, Gregory; and Yin, Deling. 2011. Β-Arrestin 2-Mediated Immune Suppression Induced by Chronic Stress. NeuroImmunoModulation. Vol.18(3). 142-149. https://doi.org/10.1159/000322868 PMID: 21228603 ISSN: 1021-7401