PURPOSE: A20 gene functions in negative immunoregulation and its SNP is related to SLE disease. But its expression level in immune cells from SLE patients is still unclear. The aim of this study is to investigate whether the expression of A20 is associated with pathogenesis of SLE. METHODS: Real-time transcription-polymerase chain reaction analysis (RT-PCR) was used to determine expression of A20 mRNA in peripheral blood mononuclear cells (PBMC) from 37 patients with SLE and 32 healthy controls. RESULTS: A20 expression was decreased in SLE patients compared with healthy controls (p = 0.0133). The expression level of A20 gene negatively correlated with the SLE disease activity index (SLEDAI) (r =-0.4661, p = 0.0036) and erythrocyte sedimentation rate (ESR) (r =-0.5222, p = 0.0009). Furthermore, SLE patients with nephritis had a lower expression of A20 than those without nephritis (p = 0.0188). CONCLUSIONS: Our results suggest that the insufficient expression of A20 gene in PBMC may take part in the pathogenesis of SLE disease.
PURPOSE:A20 gene functions in negative immunoregulation and its SNP is related to SLE disease. But its expression level in immune cells from SLEpatients is still unclear. The aim of this study is to investigate whether the expression of A20 is associated with pathogenesis of SLE. METHODS: Real-time transcription-polymerase chain reaction analysis (RT-PCR) was used to determine expression of A20 mRNA in peripheral blood mononuclear cells (PBMC) from 37 patients with SLE and 32 healthy controls. RESULTS:A20 expression was decreased in SLEpatients compared with healthy controls (p = 0.0133). The expression level of A20 gene negatively correlated with the SLE disease activity index (SLEDAI) (r =-0.4661, p = 0.0036) and erythrocyte sedimentation rate (ESR) (r =-0.5222, p = 0.0009). Furthermore, SLEpatients with nephritis had a lower expression of A20 than those without nephritis (p = 0.0188). CONCLUSIONS: Our results suggest that the insufficient expression of A20 gene in PBMC may take part in the pathogenesis of SLE disease.
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