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Cited by 118Stress Responses and CortisolTryptophan and brain disordersT-cell and B-cell Immunology

Enhanced Th17 phenotype in individuals with generalized anxiety disorder

Open access
Vieira, Morgana M.M., Ferreira, Thais B., Pacheco, Paulo A.F., Barros, Priscila O., Almeida, Carla R.M., Araújo-Lima, Carlos Fernando, Silva-Filho, Renato G., Hygino, Joana +4 more·2010·Journal of Neuroimmunology
DOI 10.1016/j.jneuroim.2010.07.018
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Abstract

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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  • Some studies have found increased circulating concentrations of TNF-α among GAD and PD patients, whereas other research has found no difference in TNF-α concentrations between anxiety disorders more generally, agoraphobia, or PD patients and controls.

    “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 been described in GAD patients.

    “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

    Section 3.2 reports significantly lower IL-2 and IL-4 release from activated cell cultures derived from people with GAD than from controls. Section 2.5 specifies that cytokines were measured in culture supernatants after in vitro stimulation, not as circulating concentrations in patients. (LLM, conf=0.90)

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  • Tumor necrosis factor-α is increased in generalized anxiety disorder (GAD) and panic disorder (PD).

    “| 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)

    The Abstract and Discussion report higher TNF-α release from activated T-cell cultures obtained from people with GAD than from controls. The finding concerns cells stimulated in vitro, not necessarily circulating TNF-α levels, and the paper does not report a corresponding finding for panic disorder. (LLM, conf=0.88)

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  • Tumor necrosis factor-α increases over time in agoraphobia.

    “| 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)

    The Discussion reports higher TNF-α release from activated cell cultures of individuals with generalized anxiety disorder. It does not report that TNF-α increases over time in agoraphobia, nor does it establish the citing table’s panic-disorder finding. (LLM, conf=0.87)

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  • In vitro activation of CD4 cells isolated from patients with generalized anxiety disorder induces them to acquire a TH17 phenotype.

    “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

    Methods §§2.2 and 2.5 describe in vitro activation of whole peripheral blood mononuclear cell cultures, followed by measurement of cytokines in their supernatants. Results §3.2 reports higher IL-17 and TNF-α after activation in cultures from patients with generalized anxiety disorder. The paper does not show that isolated CD4 cells acquired a Th17 phenotype; that is more specific than its finding. (LLM, conf=0.89)

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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)
DOI
10.1016/j.jneuroim.2010.07.018
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
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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