The role of granulocyte colony-stimulating factor in Takayasu arteritis

Previous studies have suggested that granulocyte colony-stimulating factor (G-CSF) treatment may trigger large vessel vasculitis (LVV). However, the role of G-CSF in Takayasu arteritis (TAK), a form of LVV, remains unclear. This study aims to investigate the potential role of G-CSF in TAK.

This cross-sectional study included 40 TAK patients who met the 1990 American College of Rheumatology (ACR) classification criteria for Takayasu arteritis and 27 healthy controls (HCs). Group differences and correlations between G-CSF level, clinical parameters, and cytokine profiles were analyzed using appropriate tests. Aortic tissues from TAK patients were also examined for G-CSF expression using immunohistochemistry.

G-CSF levels were significantly higher in TAK patients compared to controls (p < 0.0001), but no difference was found between active and inactive TAK. G-CSF levels positively correlated with neutrophil (R = 0.350, p = 0.028) and platelet counts (R = 0.466, p = 0.005). Elevated G-CSF levels were associated with several cytokines, including IL-6 (R = 0.672, p < 0.001), IL-17 (R = 0.692, p < 0.001), and IFN-γ (R = 0.897, p < 0.001).

G-CSF may contribute to the inflammatory process and pathogenesis of TAK, offering new perspectives for its diagnosis and treatment. Key Points • This study systematically evaluated the role of G-CSF in TAK. • G-CSF level was significantly higher in TAK patients. • G-CSF level was found to have a significant positive correlation with neutrophil and platelet counts, as well as several cytokines in TAK patients. • G-CSF may contribute to the TAK process through the PI3 K-Akt pathway.