PD-1 Deficiency in Regulatory T Cells May be Involved in the Pathogenesis of Takayasu's Arteritis

被引:0
作者
Gao, Na [1 ]
Li, Taoao [1 ]
Cui, Wei [1 ]
Zhao, Limin [1 ]
Zhang, Jianghui [1 ]
Pan, Lili [1 ,2 ]
机构
[1] Capital Med Univ, Beijing Anzhen Hosp, Beijing Inst Heart Lung & Blood Vessel Dis, Beijing, Peoples R China
[2] Capital Med Univ, Dept Rheumatol, Affiliated Anzhen Hosp, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
Takayasu's arteritis; programmed death-1; regulatory T cell;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
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页数:9
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