Investigating interferon type I responses in patients with suspected giant cell arteritis and polymyalgia rheumatica

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are closely related inflammatory disorders. Easily measurable biomarkers defining active disease and identifying patients in need of glucocorticoid sparing treatment options are highly desired. Interferon Type I (IFN-I) might be involved in disease pathology; however, evidence is limited. This study explores a systemic IFN-I signature and expression of IFN-I markers in GCA and PMR patients. Treatment naive GCA and PMR patients, and PMR patients with glucocorticoid treatment were included. Patients suspected of but not diagnosed with GCA were used as controls. Five relevant IFN-I-stimulated genes were identified in literature, and relative expression levels were determined using quantitative reverse transcription polymerase chain reaction (RT-qPCR) in peripheral blood mononuclear cells. An IFN-I score was generated. Serum levels of IFN-I induced C-X-C motif chemokine 10 (CXCL10) and Galectin-9 were determined by multiplex immunoassay. There were no differences in IFN-I scores between the groups. An IFN-I signature was observed in 0/9 controls, 2/11 GCA patients, 4/20 treatment naive PMR patients, and 2/10 PMR patients with treatment. Serum CXCL10 and Galectin-9 were not increased in GCA or PMR patients compared to control patients. Treated PMR patients had lower CXCL10 levels [423.2 pg/ml (375.1-491.1)] compared to treatment naive PMR patients [641.8 pg/ml (552.8-830.6)]. An IFN-I signature does not distinguish GCA and PMR patients from controls. Also, IFN-I-induced serum markers are not upregulated in GCA and PMR patients. Easily measurable IFN-I-induced serum markers will therefore probably not aid in diagnosis and additional treatment options in newly diagnosed GCA and PMR patients.