Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · 2023
PD-1 Deficiency in Regulatory T Cells May be Involved in the Pathogenesis of Takayasu's Arteritis.
СтатьяНазвание и аннотация: Перевод в очереди
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Gao Na, Li Taoao, Cui Wei, Zhao Limin, Zhang Jianghui, Pan Lili
Аннотация
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.
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.