摘要
The aim of this study was to investigate the expression of PD-1 on peripheral blood mononuclear cells (PBMCs) and the serum level of CXCL10 and those of roles in the pathogenesis in SLE patients. The expression of PD-1 on PBMCs was tested by flow cytometry and the serum level of CXCL10 was determined by ELISA in 47 SLE patients and 21 healthy controls. The correlation between PD-1, CXCL10 and ANA, anti-dsDNA antibody and SLEDAI (SLE disease activity index) were evaluated. The expression of PD-1 on PBMCs in SLE patients was significantly different from that of controls. The percentage of PD-1 on neutrophiles in SLE patients was decreased compared with that of healthy controls (P<0.01), and that on lymphocyte from inactive SLE was significantly lower than that of controls (P<0.02). However, the PD-1 expression and the level of serum CXCL10 in active SLE were significantly increased (P<0.01) than those of controls. Positive correlations were found between PD-1, CXCL10 and anti-dsDNA antibody, SLEDAI in active SLE. The abnormal expression of PD-1 on PBMCs and serum level of CXCL10 in SLE patients may impair the auto-immunological tolerance, and play an important role in the pathogenesis of SLE.
The aim of this study was to investigate the expression of PD-1 on peripheral blood mononuclear cells （PBMCs） and the serum level of CXCL10 and those of roles in the pathogenesis in SLE patients. The expression of PD-1 on PBMCs was tested by flow cytometry and the serum level of CXCL10 was determined by ELISA in 47 SLE patients and 21 healthy controls. The correlation between PD-1, CXCL10 and ANA, anti-dsDNA antibody and SLEDAI （SLE disease activity index） were evaluated. The expression of PD-1 on PBMCs in SLE patients was significantly different from that of controls. The percentage of PD-1 on neutrophiles in SLE patients was decreased compared with that of healthy controls （ P 〈 0.01）, and that on lymphocyte from inactive SLE was significantly lower than that of controls （ P 〈 0.02）. However, the PD-1 expression and the level of serum CXCL10 in active SLE were significantly increased （P 〈 0.01） than those of controls. Positive correlations were found between PD-1, CXCL10 and anti-dsDNA antibody, SLEDAI in active SLE. The abnormal expression of PD-1 on PBMCs and serum level of CXCL10 in SLE patients may impair the auto-immunological tolerance, and play an important role in the pathogenesis of SLE.
