ABSTRACT
Objective To analyze the expression of purinergic receptor P2X ligand-gated ion channel 7 (P2X7R) on different cells and peripheral blood mononuclear cell (PBMC) and to investigate its correlation with inflammatory cytokines in patients with SLE.Methods Flow cytometry was used to detect surface expression of P2X7R on lymphocytes,CD4+ cells,and CD19+ cell in 29 SLE patients and 28 healthy human controls to compare the difference between the SLE patients and the controls in P2X7R expression.Enzyme linked immunosorbent assay (ELISA) was performed to detect P2X7R-related serum cytokines interleukin (IL)-1β,IL-6,tumor necrosis factor (TNF)-α level.T test,Wilcoxon rank sum test,Spearman's correlation analysis were used for statitical analysis.Results ① SLE patients had significantly higher expression of P2X7R on CD4+,CD8+ lymphocytes compared to controls [CD4+ cells∶ 2.21(3.55) vs 0.89(1.15),Z=-1.527,P=0.015； CD19+ cells∶ 11.53(20.01) vs 6.66 (6.27),Z=-2.091,P=0.037]； ② The levels of three cytokines in patients with SLE were significantly higher than those in control.The positive relationship between P2X7R expression in lymphocytes with the serum IL-6 level was found in SLE patients (r=0.449,P=0.015)；③ Patients with arthritis showed significantly higher expression of P2X7R on lym-phocytes compared to patients without arthritis (Z=-2.772,P=0.006).The expression of P2X7R on lymphocytes and CD19+ cell was significantly positively correlated with the SLEDAI score.Positive correlation with anti-β2GP Ⅰ in lymphocyteswas also found.Conclusion P2X7R may mediate the release of inflammatory cytokines involved in the pathogenesis of SLE,and may participate the development of arthritis,lupus nephritis and NPSLE in SLE patients.
ABSTRACT
Objective To investigate the frequencies of CD4+CXCR5+T cells in the CD4+T cells of peripheral blood of patients with systemic lupus erythematosus (SLE) and the effect of glucocorticoid on it.Methods Frequencies of CD4+CXCR5+T cell were analyzed by flow cytometry in 45 active,20 inactive SLE patients and 20 healthy controls.Differences between groups and the effect of glucocorticoid were analyzed.Meanwhile, the expression of CXCR5 on CDI9+B cells was analyzed. Independent sample t test was used for statistical analysis between twogroups, ANOVA was applied for data analysis between 3 groups,,nonparameterical Spearman's analysis was used for correlation analysis and repeated measurement ANOVA were used to compare the parameters before and after treatment. Results The percentage of CD4+CXCR5+ in CD4+T cells was increased in patients with SLE compared with healthy controls[(16±7)% vs (12±3)%, P＜0.01].It was increased in patients with active SLE [(18±7)%] compared with healthy controls (P＜0.05) but there was no significant difference between inactive SLE[(11±4)%] and healthy controls(P＞0.05). The percentage in patients with LN was higher than that in patients without LN, but without significant difference[(18±7)%vs (14±7)%, P=0.05 ]. The percentage of CD4+CXCR5+T cells was positively correlated with SLEDAI,the titer of ANA and level of ESR but negatively correlated with the level of C3 (P<0.05 for each).No correlation was found between duration and the levels of CRP and immunoglobulin.. The percentage in patients with high anti-dsDNA group was also higher than that of the low group, but no differences were found between anti-Sm antibody positive and negative groups neither between anti-SSA/SSB antibody positive and negative groups(P＞0.05 for each).The expression level of CXCR5 on CD19+B cells in active SLE patients was lower than that of healthy controls[(85±11)% vs (94±3)%, P＜0.05 ]. The percentages of CD4+CXCR5+T cells in 10 untreated active SLE patients were decreased at day 1,day 3 and day 7 after being treated with dexamethasone (20mg/d) when compared with those before the treatment (P＜0.05 for each), but the percentages of CD19+CXCR5+B cells had no significant change (P＞0.05 for each).Conclusion These results demonstrate that the abnormality of CD4+CXCR5+T cells may play an important role in the pathogenesis of SLE.