Vasculitis & polymyalgia rheumatica
Crosstalk between macrophages and fibroblasts contributes to inflammation and damage in giant cell arteritis
Authors' conclusion
The interaction between fibroblasts and macrophages may contribute to the chronicity and progression of GCA and deserves further investigation. Serum tenascin-C is a candidate biomarker for GCA diagnosis.
Study context
- Population
- Giant cell arteritis (GCA)-positive temporal arteries and aorta tissues; GCA patients and healthy controls; monocytes from healthy donorsGCA-positive temporal arteries 9 · aorta tissues 9 · healthy donors 10
- Participants
- 36 vs 46
- Comparison
- GM-CSF- vs M-CSF-macrophage-conditioned medium on aortic adventitial fibroblasts; serum tenascin-C in GCA vs healthy controls
- GCAn = 36
- Healthy controlsn = 46reference
Methodological detailsimmunostaining of GCA-affected arteries, in vitro macrophage–fibroblast co-culture (conditioned medium), serum ELISA
- Immunostaining of GCA-affected arteries
- In vitro macrophage–fibroblast co-culture (conditioned medium)
- Serum ELISA
Main finding
As reported in the abstract
- In GCA arteries, pro-inflammatory CD90+IL-6+ fibroblasts, but not pro-resolving CD90+CD200+ fibroblasts, spatially associated with macrophages
- Adventitial CD90+ fibroblasts expressed GM-CSF and/or M-CSF, linked to macrophage subset distribution
- GM-CSF- and, to a lesser extent, M-CSF-derived MCM upregulated fibroblast mRNA of IL-6, GM-CSF, M-CSF, CCL2, PDPN and CD200
- GM-CSF-derived MCM upregulated IL-1β, MMP-3, Col3a1 and tenascin-C and downregulated FAP in fibroblasts
- Adventitial CD90+ fibroblasts in GCA temporal arteries also expressed MMP-3 and tenascin-C
- Serum tenascin-C significantly higher in treatment-naïve GCA than healthy controls
Further findings
- Diagnostic accuracy of serum tenascin-C for GCA
- 0.89 · AUC
Original publication
Crosstalk between macrophages and fibroblasts contributes to inflammation and damage in giant cell arteritis. Rheumatology (Oxford). Published 7 August 2025. doi:10. 1093/ rheumatology/ keaf408
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