Cited by 33Systemic Lupus Erythematosus ResearchPsoriasis: Treatment and PathogenesisT-cell and B-cell Immunology

Glucocorticoids enhance Th17/Th1 imbalance and signal transducer and activator of transcription 3 expression in systemic lupus erythematosus patients

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Prado, Catuxa, de Paz, Banesa, Gómez, Jesús, López, Patricia, Rodríguez-Carrio, Javier, Suárez, Ana·2011·Rheumatology

Abstract

OBJECTIVE: To investigate the relative amounts of Th17 and Th1 cells present in SLE patients and the possible effects of treatments or disease features on these populations. METHODS: Peripheral blood mononuclear cells were collected from 75 SLE patients and 19 healthy controls and the proportion of Th17 and Th1 populations were assessed by flow cytometry measuring the amount of IL-17 and IFN-γ-producing cells. Gene expression of signal transducers and activators of transcription 3 (STAT3), STAT4, IL-6R and IL-12R were determined in 30 patients and 8 healthy individuals by real-time RT-PCR. Data were related to clinical and immunological parameters and to the treatment followed during the past 3 months. RESULTS: Th17 cells and the Th17/Th1 ratio were significantly increased in SLE patients treated with glucocorticoids compared with healthy individuals, untreated patients or those under other treatments. No association was detected with clinical parameters, but patients with anti-ENA antibodies also displayed increased Th17 responses. Disease activity (SLEDAI) is associated with the Th17/Th1 index only in glucocorticoid-treated patients. In line with these results, gene expression of STAT3 and IL-6R was up-regulated in patients taking these drugs. Accordingly, we found a positive correlation between the Th17/Th1 ratio and STAT3 levels. CONCLUSIONS: The present work provides the first evidence that aberrant Th17/Th1 balance in SLE is linked to the use of glucocorticoids and suggests that the up-regulatory effect of these drugs on the Th17 population could be associated with their ability to increase STAT3 and IL-6R expression. Additionally, anti-ENA positivity could represent a potential biomarker for Th17 bias.

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Crossref · 10.1093/rheumatology/ker227

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Authors
Prado, C., de Paz, B., Gómez, J., López, P., Rodríguez-Carrio, J., & Suárez, A.
Affiliations
  • Universidad de Oviedo (ES)
  • Consejo Superior de Investigaciones Científicas (ES)
Venue
Rheumatology
Published
2011-07-12
Volume
50
Issue
10
Pages
1794-1801
ISSN
  • 1462-0324 (ISSN-L)
  • 1462-0332
OpenAlex
W2115027742
Cited by
33
References
36
Citations by year
2026: 1 · 2025: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 1 · 2015: 4 · 2014: 6 · 2013: 3 · 2012: 4
FWCI
3.27
Type
journal article
Language
en
Open access
Licence
cc-by-nc-nd
Locations
  • Lara D. Veeken (publishedVersion)
  • PubMed (publishedVersion)
  • Consultation of the Doctoral Thesis Database (TESEO) (Ministerio de Educación, Cultura y Deporte) (submittedVersion, cc-by-nc-nd)
  • DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
Funders
European Commission
Topics
  • Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
systemic lupus erythematosus, glucocorticoids, Th17 cells, Th1 cells, STAT3, STAT4, IL-6 receptor, IL-12 receptor, anti-ENA antibodies, disease activity, immunosuppressive therapy, biomarkers
MeSH terms
Adult, Drug Therapy, Combination, Female, Glucocorticoids, Humans, Immunosuppressive Agents, Interferon-gamma, Ionophores, Leukocyte Count, Leukocytes, Mononuclear, Lupus Erythematosus, Systemic, Male, Tetradecanoylphorbol Acetate, Th1 Cells, Interleukin-17, STAT3 Transcription Factor, Th17 Cells

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