OBJECTIVE: To investigate the level of FOXP3 expressed in CD4+ CD39+ T cells in peripheral blood of patients with systemic lupus erythematosus (SLE) and observe the regulation of glucocorticoid on it. METHODS: Frequencies of CD4+ CD25+ CD39+, CD4 CD25+ FOXP3+ and CD4+ CD39+ FOXP3+ T cells and levels of FOXP3 protein were analyzed by flow cytometry of 47 SLE patients (including 29 untreated/active SLE) and 22 healthy controls. Meanwhile, correlations among three groups and influences of glucocorticoid were analyzed. RESULTS: Percents of CD4+ CD25+ CD39+ T cells expressed in active SLE, inactive SLE and healthy controls were (1.3 +/- 0.5)%, (1.9 +/- 0.8)% and (2.3 +/- 1.0)% respectively, the level decreased in active SLE compared with inactive SLE and healthy controls P < 0.05 in each group, but it had no significant difference between the latter two groups (P > 0.05). In active SLE, levels of FOXP3 protein expressed in CD4+ CD25+, CD4+ CD25high and CD4+ CD39+ T cells were (45 +/- 12)%, (65 +/- 14)% and (70 +/- 14)% respectively. Levels of FOXP3 expressed in CD4+ CD25high and CD4+ CD39+ T cells were higher than that expressed in CD4+ CD25+ T cells (P < 0.01), while it had no significant difference between CD4 CD25high T cells and CD4+ CD39+ T cells (P > 0.05). CONCLUSIONS: These results demonstrate that CD39 may be a better surface marker of regulatory T cells, and that deficiency of CD39+ Treg cells may play an important role in the pathogenesis of SLE.
OBJECTIVE: To investigate the level of FOXP3 expressed in CD4+ CD39+ T cells in peripheral blood of patients with systemic lupus erythematosus (SLE) and observe the regulation of glucocorticoid on it. METHODS: Frequencies of CD4+ CD25+ CD39+, CD4CD25+ FOXP3+ and CD4+ CD39+ FOXP3+ T cells and levels of FOXP3 protein were analyzed by flow cytometry of 47 SLEpatients (including 29 untreated/active SLE) and 22 healthy controls. Meanwhile, correlations among three groups and influences of glucocorticoid were analyzed. RESULTS: Percents of CD4+ CD25+ CD39+ T cells expressed in active SLE, inactive SLE and healthy controls were (1.3 +/- 0.5)%, (1.9 +/- 0.8)% and (2.3 +/- 1.0)% respectively, the level decreased in active SLE compared with inactive SLE and healthy controls P < 0.05 in each group, but it had no significant difference between the latter two groups (P > 0.05). In active SLE, levels of FOXP3 protein expressed in CD4+ CD25+, CD4+ CD25high and CD4+ CD39+ T cells were (45 +/- 12)%, (65 +/- 14)% and (70 +/- 14)% respectively. Levels of FOXP3 expressed in CD4+ CD25high and CD4+ CD39+ T cells were higher than that expressed in CD4+ CD25+ T cells (P < 0.01), while it had no significant difference between CD4 CD25high T cells and CD4+ CD39+ T cells (P > 0.05). CONCLUSIONS: These results demonstrate that CD39 may be a better surface marker of regulatory T cells, and that deficiency of CD39+ Treg cells may play an important role in the pathogenesis of SLE.