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Updated: May 2, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 27, 2013
Th17 and Th1 T-cell responses in giant cell arteritis
Jiusheng Deng1, Brian R Younge, Richard A Olshen
1Division of Immunology and Rheumatology, Stanford University School of Medicine, 269 W Campus Dr, Stanford, CA 94305, USA.
Glucocorticoids suppress Th17 cells in giant cell arteritis (GCA) but not Th1 cells. Targeting persistent Th1 responses is crucial for resolving chronic vasculitis and monitoring T cell frequencies can assess GCA activity.
Area of Science:
- Immunology
- Rheumatology
- Vascular Biology
Background:
- Giant cell arteritis (GCA) involves systemic inflammation and aortic damage.
- Glucocorticoids are standard treatment but do not eliminate vessel wall infiltrates.
- The precise effects of glucocorticoids on GCA's systemic and vascular aspects remain unclear.
Purpose of the Study:
- To investigate the impact of glucocorticoids on immune cell profiles in GCA.
- To understand the differential effects of glucocorticoids on Th17 and Th1 pathways in GCA.
Main Methods:
- Examined immune cell profiles in blood and temporal artery biopsies from GCA patients.
- Utilized flow cytometry, qPCR, and immunohistochemistry for analysis.
- Employed human artery-mouse chimeras to model GCA vascular inflammation.
Main Results:
- Elevated plasma interferon-gamma (IFN-γ) and interleukin-17 (IL-17) with increased T cell frequencies pre-treatment.
- Glucocorticoids suppressed Th17 cells and Th17-promoting cytokines (IL-1β, IL-6, IL-23) but spared Th1 cells and Th1-promoting cytokines (IL-12).
- This selective suppression was observed in both circulation and temporal artery biopsies, and in a humanized mouse model.
Conclusions:
- Two pathways, Th17 and Th1 cells, drive GCA pathogenesis.
- IL-17-producing Th17 cells are glucocorticoid-sensitive, while IFN-γ-producing Th1 responses persist.
- Targeting steroid-resistant Th1 responses is necessary for chronic GCA, and monitoring Th17/Th1 frequencies may aid disease assessment.
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