Dopamine up-regulates Th17 phenotype from individuals with generalized anxiety disorder

被引:31
作者
Ferreira, Thais B. [1 ]
Kasahara, Taissa M. [1 ]
Barros, Priscila O. [1 ]
Vieira, Morgana M. M. [1 ]
Bittencourt, Vera Carolina B. [1 ]
Hygino, Joana [1 ]
Andrade, Regis M. [1 ]
Linhares, Ulisses C. [1 ]
Andrade, Arnaldo F. [2 ]
Bento, Cleonice A. [1 ]
机构
[1] Fed Univ State Rio Janeiro, Dept Microbiol & Parasitol, BR-20261040 Rio De Janeiro, Brazil
[2] State Univ Rio Janeiro, Dept Microbiol, Rio De Janeiro, Brazil
关键词
Generalized anxiety disorder; Th17/Th1; IL-10/TGF-beta; Dopamine; Glucocorticoid; POSTTRAUMATIC-STRESS-DISORDER; PRO-INFLAMMATORY CYTOKINES; RECEPTOR MESSENGER-RNA; CD4+AND CD8+T CELLS; T-CELLS; BLOOD-LYMPHOCYTES; IMMUNE-SYSTEM; TNF-ALPHA; IN-VITRO; EXPRESSION;
D O I
10.1016/j.jneuroim.2011.06.009
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Our objective was to evaluate the effect of stress-related dose of dopamine (DA) on the in vitro proliferation and cytokine production in polyclonally-activated T cells from healthy individuals or individuals with generalized anxiety disorder (GAD). Our results demonstrated that cell cultures from GAD group proliferated less following T cell activation, as compared with control group. The addition of DA reduced the proliferative response in cell cultures from healthy but not from GAD individuals. The cytokine profile in GAD individuals revealed Th1 and Th2 deficiencies associated with a dominant Th17 phenotype, which was enhanced by DA. A similar DA-induced immunomodulation was also observed in PPD-activated cell cultures from GAD individuals. Unlike the control, DA-enhanced Th17 cytokine production in GAD individuals was not affected by glucocorticoid. In conclusion, our results show that the T cell functional dysregulation in GAD individuals is significantly amplified by DA. These immune abnormalities can have impact in increasing the susceptibility of individuals with anxiety disorders to infectious diseases and inflammatory/autoimmune disorders. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:58 / 66
页数:9
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