Meng Shuai1,2, Yan Ni3, Xu Jian3, Shuangtao He3, Jin-An Zhang4,3. 1. Department of Endocrinology, Zhejiang Hospital, Hangzhou, Zhejiang, People's Republic of China. momingfd@163.com. 2. Department of Endocrinology, Jinshan Hospital of Fudan University, Shanghai, People's Republic of China. momingfd@163.com. 3. Department of Endocrinology, Jinshan Hospital of Fudan University, Shanghai, People's Republic of China. 4. Department of Endocrinology and Rheumatology, Shanghai University of Medicine & Health Sciences Affiliated Zhoupu Hospital, Shanghai, People's Republic of China.
Abstract
INTRODUCTION: The aim of this study was to explore the potential role of IL-35 in Graves' disease (GD). MATERIAL AND METHODS: A total of 142 GD patients including 80 newly onset patients, 52 refractory patients and 10 remission patients and 70 normal controls (NCs) were recruited. The messenger RNA (mRNA) expressions of P35 and Epstein-Barr-virus-induced gene 3 (Ebi3) were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Serum level of IL-35 was measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The expression of IL-35mRNA in new onset GD and refractory GD were both significantly higher than NC. Comparison between remission GD and NC showed no significant difference (p > 0.05). A significant increase of Ebi3mRNA expression was observed in new onset GD compared with remission GD (p = 0.030). The new onset GD showed a tendency for increased expression of serum IL-35 but without significant difference. No correlation between IL-35 expression and clinic parameters was found. CONCLUSIONS: Our preliminary observations indicate that IL-35 and CD4+P35+Ebi3+T cells may be involved in the pathogenesis of GD.
INTRODUCTION: The aim of this study was to explore the potential role of IL-35 in Graves' disease (GD). MATERIAL AND METHODS: A total of 142 GDpatients including 80 newly onset patients, 52 refractory patients and 10 remission patients and 70 normal controls (NCs) were recruited. The messenger RNA (mRNA) expressions of P35 and Epstein-Barr-virus-induced gene 3 (Ebi3) were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Serum level of IL-35 was measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The expression of IL-35mRNA in new onset GD and refractory GD were both significantly higher than NC. Comparison between remission GD and NC showed no significant difference (p > 0.05). A significant increase of Ebi3mRNA expression was observed in new onset GD compared with remission GD (p = 0.030). The new onset GD showed a tendency for increased expression of serum IL-35 but without significant difference. No correlation between IL-35 expression and clinic parameters was found. CONCLUSIONS: Our preliminary observations indicate that IL-35 and CD4+P35+Ebi3+T cells may be involved in the pathogenesis of GD.