ArticleMolecular medicine (Cambridge, Mass.)2025
Increased expression of Toll-like receptors and associated alarmins in temporal arteries of patients with giant cell arteritis.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Plasma proteome differences between giant cell arteritis and polymyalgia rheumatica: a pilot study.Arthritis research & therapy · 2026Article
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Abstract
backgroundGiant cell arteritis (GCA) is a chronic granulomatous inflammatory disease involving large- and medium-sized arteries. The disease spectrum comprises cranial (C-GCA), extracranial (EC-GCA) and mixed phenotypes. Toll-like receptors (TLRs) in the affected arteries may play an important role in GCA pathogenesis. However, data on TLR and TLR-ligands expression pattern in GCA arteries are lacking.
objectiveTo investigate the expression of TLRs and putative ligands in temporal artery biopsies (TAB) from C-GCA, EC-GCA and isolated polymyalgia rheumatica (PMR) patients to establish a link between TLRs, antigen expression, and disease stage. To correlate the plasma levels of identified TLR-ligands with standard inflammatory markers (IL-6, CRP, ESR) in these patients.
methodsImmunofluorescence staining of TLR2/4/7/8, HMGB-1, SAA, fibrinogen, and p-glycoprotein was performed with TABs of six biopsy proven C-GCA, six EC-GCA, five PMR patients and seven age-matched controls. Association studies among plasma inflammatory markers were done with 139 PMR and 40 GCA patients.
resultsThe levels of TLR2/4/7/8 and the alarmins HMGB-1, SAA, and fibrinogen were highly increased in C-GCA TABs in the sites of inflammation and less in EC-GCA TABs. P-glycoprotein was overexpressed in C-GCA TABs. Glucocorticoids or TAK1-inhibitor treatment decreased the fibrinogen- and SAA-mediated IL-6 production in control PBMCs. Plasma levels of SAA and fibrinogen associated strongly with CRP and ESR levels.
conclusionTLRs are overexpressed at the site of vascular inflammation in C-GCA and at a lower level in EC-GCA and PMR with negative TAB. Moreover, HMGB-1, SAA, and fibrinogen may serve as disease biomarkers of patients with C-GCA.
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