English Abstract
Journal Article
Research Support, Non-U.S. Gov't
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[Study of fas-mediated Foxp3+CD4+CD25+ Treg cell apoptosis in patients with systemic lupus erythematosus].

OBJECTIVE: To explore the role of fas apoptosis signal transduction pathway in the abnormal apoptosis of Foxp3+CD4+CD25+ Treg in patients with systemic lupus erythematosus (SLE).

METHODS: Twenty-five active SLE patients, 20 remission SLE patients and 25 controls were selected. The level of fas expression on peripheral blood Foxp3+CD4+CD25+ Treg surface was detected in SLE patients. And analyzed the expression rate of Foxp3 on CD4+CD25+ T cells was analyzed to explore the relationship between the expression rate and disease activity.

RESULTS: (1) The expression rate of fas on Foxp3+CD4+CD25+ Treg was (23.72 ± 2.35)%, (14.0 ± 2.1)% in active and remission SLE groups respectively versus (10.1 ± 1.2)% in control group. The fas expression rate of active SLE group was significantly higher than those of remission SLE group(P < 0.01)and control group (P < 0.01). And the remission SLE and control groups were not statistically significant (P > 0.05). The expression rate of fas on the Foxp3+CD4+ CD25+ Treg was positively correlated with the SLEDAI (SLE disease activity index) score (r = 0.336, P < 0.05). (2) The expression rate of Foxp3 on CD4+CD25+ T cells was (2.83 ± 0.30)%, (5.38 ± 0.63)% in active and remission SLE groups respectively versus (8.12 ± 0.70)% in control group. The expression rate of Foxp3 was significantly lower in active SLE group than that in remission SLE group (P < 0.01)and control group (P < 0.01). And the Foxp3 expression rate of remission group was also lower than that of control group (P < 0.05). The expression rate of Foxp3 was negatively correlated with the SLEDAI score (r = -0.581, P < 0.01). (3) The expression rate of Foxp3 was negatively correlated with fas (r = -0.349, P < 0.01).

CONCLUSION: The abnormal apoptosis of Foxp3+CD4+CD25+ Treg mediated by the fas apoptosis signal transduction pathway may be one of the pathogenic mechanisms of disease activity in SLE patients.

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