Abstract
OBJECTIVES: This study aims to investigate whether PD-1 expressions are abnormal in patients with TAK. METHODS: PD-1 expression was analyzed by flow cytometry. Serum cytokines IL-10, IL-7, IL-2, IL-15, CCL2, CCL3, and CXCL10 were detected using a cytokine cytometric bead array. Immunohistochemistry staining analysis was used to test PD-1 and programmed death-ligand 1 (PD-L1) expression in the aorta of three patients with TAK and three patients with atherosclerosis as controls. RESULTS: The mean fluorescence intensity of PD-1 in CD4(+)PD-1(+) cells was decreased in patients with TAK and the frequency of CD4(+)Foxp3(-)PD-1(+) cells among CD4(+)T cells was also decreased in peripheral blood relative to healthy controls (P < .05). The percentage of CD4(+)CD25(+)Foxp3(+)PD-1(+) cells in the CD4(+)CD25(+)T cell population was lower in patients with TAK than in healthy control and was lower in active TAK group (P < .05). Comparing PD-1 and PDL-1 expression in aorta tissue showed that patients with TAK tended to have lower levels than patients with atherosclerosis, but the difference was not significant (P > .05). Patients with TAK had higher serum levels of IL-10, IL-7, CCL2, and CCL3 (P < .05). CONCLUSIONS: Abnormal expression of PD-1 in serum and aorta tissue of patients with TAK may contribute to TAK pathogenesis. KEY POINTS: PD-1 expression in both peripheral blood and aorta tissue of TAK patients decreased relative to healthy controls, indicating that PD-1 might be involved in TAK pathogenesis.