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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
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In Synergy With Interferon-γ, Interleukin-17 Activates Vascular Stromal Cells Toward a Proinflammatory Profile in
Hélène Greigert1,2,3, André Ramon3,4, Claudie Cladiere1,3
1Department of Internal Medicine and Clinical Immunology, Referral Center for Rare Systemic Autoimmune and Autoinflammatory Diseases, Dijon University Hospital, Université EPE Bourgogne Europe, Dijon, France.
Arthritis & Rheumatology (Hoboken, N.J.)
|January 12, 2026
Summary
Interleukin-17 (IL-17) drives vascular inflammation in Giant Cell Arteritis (GCA) by activating myofibroblasts. This activation, amplified by IFN-γ, increases pro-inflammatory factors, highlighting IL-17
Area of Science:
- Immunology
- Vascular Biology
- Rheumatology
Background:
- The role of Interleukin-17 (IL-17) in Giant Cell Arteritis (GCA) pathogenesis remains unclear, despite evidence implicating T helper 17 (Th17) cells.
- Understanding IL-17's specific contribution is crucial for developing targeted therapies for GCA, a serious inflammatory condition affecting large arteries.
Purpose of the Study:
- To elucidate the precise role of IL-17 in GCA pathogenesis.
- To investigate the effects of IL-17 on vascular cells, specifically myofibroblasts (MFs), and its interaction with other inflammatory mediators like IFN-γ.
Main Methods:
- Ex vivo culture of temporal artery biopsies (TABs) from GCA patients with IL-17 or secukinumab (an IL-17 inhibitor).
- Analysis using bulk RNA-sequencing, RT-qPCR, and confocal microscopy to assess gene expression and protein localization.
- In vitro co-culture systems involving MFs and peripheral blood mononuclear cells to study T-cell polarization and cellular responses.
Main Results:
- Secukinumab treatment reduced expression of vascular inflammation genes (e.g., IL6) in GCA TABs.
- IL-17 upregulated pro-inflammatory genes (IL-6, CCL20, GM-CSF) in MFs, an effect reversed by secukinumab.
- IL-17 receptor expression on MFs was enhanced by IFN-γ, leading to synergistic pro-inflammatory cytokine production and promoting Th17 polarization.
Conclusions:
- IL-17 significantly exacerbates vascular inflammation in GCA by activating MFs.
- Synergy between IL-17 and IFN-γ amplifies the production of key inflammatory mediators, implicating IL-17 as a critical driver of GCA pathogenesis.
- Targeting IL-17 may offer a therapeutic strategy for managing GCA.
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