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Enhanced Th17 phenotype in individuals with generalized anxiety disorder
Open accessAbstract
The generalized anxiety disorder (GAD) is often a debilitating chronic condition, characterized by long-lasting anxiety that is not focused on any object or situation. Besides being clearly linked to increased susceptibility to infectious diseases, anxiety is also known to contribute to the pathogenesis of many inflammatory/autoimmune disorders. The present work aimed to explore the T cell profile following in vitro activation in cultures obtained from a group of individuals with GAD, comparing them with healthy control individuals. Our results demonstrated that cell cultures from GAD group proliferated less following T cell activation as compared with the control group. The analysis of the cytokine profile revealed Th1 and Th2 cytokine deficiencies in the anxious group, as compared with the control subjects. On the other hand, this cellular and humoral immune damage was followed by enhanced production of Th17-derived cytokines. In particular, the levels of TNF-α and IL-17 were significantly higher in cell cultures containing activated T cells from GAD individuals. Therefore, besides a deficiency on Th1 phenotype, an elevated proinflammatory status of these individuals might be related to both glucocorticoid immune resistance and lower IL-10 levels produced by activated T cells. In conclusion, our results demonstrated a T cell functional dysregulation in individuals with GAD, and can help to explain the mechanisms of immune impairment in these subjects and their relationship with increased susceptibility to infections and autoimmune diseases.
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“For example, some studies have found increased circulating concentrations of TNF-α among GAD (Vieira et al, 2010) and PD patients (Hoge et al, 2009), whereas other research has found no difference in TNF-α concentrations between anxiety disorders more generally (Vogelzangs et al, 2013), agoraphobia (Wagner et al, 2015) or PD patients and controls (Brambilla et al, 1999).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Vieira et al, 2010
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“Lower circulating concentrations of anti-inflammatory cytokines such as IL-2 and IL-4 have also been described in GAD patients (Vieira et al, 2010).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Vieira et al, 2010
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“| Tumor necrosis factor-α | Increased in GAD and PD | Hoge et al (2009),Vieira et al (2010), and Wagner et al (2015) |”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Vieira et al (2010)
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“| Tumor necrosis factor-α | Increased in GAD and PD | Hoge et al (2009),Vieira et al (2010), and Wagner et al (2015) |”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Vieira et al (2010)
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“in vitro activation of CD4 cells isolated from patients with generalized anxiety disorder induces them to acquire a TH17 phenotype (Ferreira et al., 2011; Vieira et al., 2010)”
From Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression (2018) · cites this paper as Vieira et al., 2010
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“Interestingly, lower levels of the pro-inflammatory cytokine IFN-γ have been found in both GAD and PD patients (Tukel et al, 2012;Vieira et al, 2010).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Vieira et al, 2010
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“| Interleukin-2 | Decreased in GAD | Koh and Lee (2004),Rapaport and Stein (1994), and Vieira et al (2010) |”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Vieira et al (2010)
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“| Interleukin-2 | Decreased in GAD | Koh and Lee (2004),Rapaport and Stein (1994), and Vieira et al (2010) |”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Vieira et al (2010)
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Metadata
- Authors
- Vieira, M. M. M., Ferreira, T. B., Pacheco, P. A. F., Barros, P. O., Almeida, C. R. M., Araújo-Lima, C. F., Silva-Filho, R. G., Hygino, J., Andrade, R. M., Linhares, U. C., Andrade, A. F. B., & Bento, C. A. M.
- Affiliations
- Universidade Federal do Estado do Rio de Janeiro (BR)
- Universidade do Estado do Rio de Janeiro (BR)
- Corresponding author
- Bento, Cleonice A.M.
- ORCID
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2010-12
- Volume
- 229
- Issue
- 1-2
- Pages
- 212-218
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W2046420685
- Cited by
- 118
- References
- 114
- Citations by year
- 2026: 10 · 2025: 14 · 2024: 10 · 2023: 9 · 2022: 14 · 2021: 9 · 2020: 7 · 2019: 7 · 2018: 10 · 2017: 8 · 2016: 5 · 2015: 4 · 2014: 4 · 2013: 4
- FWCI
- 0.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- generalized anxiety disorder, Th17 cells, T cell activation, TNF-α, IL-17, IL-10, glucocorticoid resistance, T cell proliferation, autoimmune disease susceptibility, infection susceptibility
- MeSH terms
- Adolescent, Adult, Anxiety Disorders, Cell Count, Dexamethasone, Enzyme-Linked Immunosorbent Assay, Female, Glucocorticoids, Humans, Lymphocyte Activation, Male, Phenotype, Tetrazolium Salts, Tumor Necrosis Factor-alpha, Interleukin-7, Cytokines, Statistics, Nonparametric, Young Adult, Th17 Cells
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