OBJECTIVE: To investigate the expression of glucocorticoid-induced tumor necrosis factor receptor (GITR) and apoptosis of CD4(+)CD25(+)CD127(dim/-) T cells of the patients with systemic lupus erythematosus (SLE),and to analyze its clinical value. METHODS: A total of 28 patients with a diagnosis of SLE according to the American College of Rheumatology (ACR) 1997 criteria were included in the study. The SLE patients were divided into active group (SLEDAI≥10) and inactive group (SLEDAI<10) according to the SLE disease activity index (SLEDAI). Active group included 15 patients and inactive group 13 patients. Clinical and laboratory data of the patients with SLE were recorded. In this study 12 normal volunteers without history of autoimmune diseases were also included. Peripheral blood CD4(+)CD25(+)CD127(dim/-) T cells were isolated by magnetic beads sorting. We classified them into two subgroups: the blank group and the therapeutic dose group (dexamethasone dose was 5×10(-2) mg/L and the peripheral blood CD4(+)CD25(+)CD127(dim/-) T cells with dexamethasone were cultured for 48 hours). The expressions of GITR and Annexin V were analyzed by flow cytometry before and after the culture. The correlations between GITR levels, apoptosis rates of these subsets and the clinic, laboratory parameters of SLE were analyzed. RESULTS: GITR levels and apoptosis rates in the patients with SLE were significantly higher than those in the normal control group (P=0.016; P=0.049). The expression levels of GITR on Treg cells between the blank group and the therapeutic dose group were found be of no significant difference in the patients with SLE (P>0.05), but in the normal group, the expression levels of GITR in the therapeutic dose group were higher than those in the blank group (P=0.034). After adding dexamethasone, the apoptosis rates of Treg cells were decreased in the patients with SLE, the difference was statistically significant (P=0.033); But in the normal control group, the apoptosis rate of Treg cells was higher in the therapeutic dose group than in the blank group (P=0.012). The expression levels of GITR on Treg cells were significantly positively correlated with SLEDAI, but were correlated negatively with the C3. CONCLUSION: The GITR is pathologically expressed on Treg cells in SLE, which may be used as an immunological index of SLE disease activity; Glucocorticoids may regulate immune abnormalities in patients with SLE by inhibiting the apoptosis of Treg cells.
OBJECTIVE: To investigate the expression of glucocorticoid-induced tumor necrosis factor receptor (GITR) and apoptosis of CD4(+)CD25(+)CD127(dim/-) T cells of the patients with systemic lupus erythematosus (SLE),and to analyze its clinical value. METHODS: A total of 28 patients with a diagnosis of SLE according to the American College of Rheumatology (ACR) 1997 criteria were included in the study. The SLEpatients were divided into active group (SLEDAI≥10) and inactive group (SLEDAI<10) according to the SLE disease activity index (SLEDAI). Active group included 15 patients and inactive group 13 patients. Clinical and laboratory data of the patients with SLE were recorded. In this study 12 normal volunteers without history of autoimmune diseases were also included. Peripheral blood CD4(+)CD25(+)CD127(dim/-) T cells were isolated by magnetic beads sorting. We classified them into two subgroups: the blank group and the therapeutic dose group (dexamethasone dose was 5×10(-2) mg/L and the peripheral blood CD4(+)CD25(+)CD127(dim/-) T cells with dexamethasone were cultured for 48 hours). The expressions of GITR and Annexin V were analyzed by flow cytometry before and after the culture. The correlations between GITR levels, apoptosis rates of these subsets and the clinic, laboratory parameters of SLE were analyzed. RESULTS:GITR levels and apoptosis rates in the patients with SLE were significantly higher than those in the normal control group (P=0.016; P=0.049). The expression levels of GITR on Treg cells between the blank group and the therapeutic dose group were found be of no significant difference in the patients with SLE (P>0.05), but in the normal group, the expression levels of GITR in the therapeutic dose group were higher than those in the blank group (P=0.034). After adding dexamethasone, the apoptosis rates of Treg cells were decreased in the patients with SLE, the difference was statistically significant (P=0.033); But in the normal control group, the apoptosis rate of Treg cells was higher in the therapeutic dose group than in the blank group (P=0.012). The expression levels of GITR on Treg cells were significantly positively correlated with SLEDAI, but were correlated negatively with the C3. CONCLUSION: The GITR is pathologically expressed on Treg cells in SLE, which may be used as an immunological index of SLE disease activity; Glucocorticoids may regulate immune abnormalities in patients with SLE by inhibiting the apoptosis of Treg cells.