Nakashima Hitoshi, Matsuno Sawako, Akahoshi Mitsuteru, Miyake Katsuhisa, Inoue Yasushi, Tanaka Yosuke, Ninomiya Ichiro, Shimizu Sakiko, Igawa Takashi, Sadanaga Atsushi, Otsuka Takeshi, Harada Mine
Department of Medicine and Biosystemic Science, Graduate School of Medical Science, Kyushu University, Maidashi 3-1-1, 812-8582 Higashi-ku, Fukuoka, Japan.
Clin Rheumatol. 2005 Feb;24(1):38-40. doi: 10.1007/s10067-004-0966-8. Epub 2004 Jul 20.
Systemic lupus erythematosus (SLE) is characterized by multisystem inflammation and production of autoantibodies, which can generate immune complexes and may cause tissue damage through the recognition of an autoantigen. Although many factors have been proposed, such as genetic factors, environmental factors, hormonal action, viruses, and dysregulation of cytokine production, the cause of this disease is not well understood. It has been reported that the levels of interferon (IFN)-alpha in the sera of some SLE patients are elevated and that IFN-alpha induces maturation of monocytes into highly active antigen-presenting dendritic cells (DCs). We analyzed the association between IFN-alpha genotype and the risk of SLE to clarify whether IFN-alpha plays a central role in susceptibility to SLE. The results showed that no IFN-alpha genotype was significantly associated with the risk of SLE.
系统性红斑狼疮(SLE)的特征是多系统炎症和自身抗体的产生,这些自身抗体可形成免疫复合物,并可能通过识别自身抗原而导致组织损伤。尽管已经提出了许多因素,如遗传因素、环境因素、激素作用、病毒以及细胞因子产生失调等,但这种疾病的病因仍未完全清楚。据报道,一些SLE患者血清中的α干扰素(IFN)水平升高,且IFN-α可诱导单核细胞成熟为高活性的抗原呈递树突状细胞(DCs)。我们分析了IFN-α基因型与SLE风险之间的关联,以阐明IFN-α是否在SLE易感性中起核心作用。结果表明,没有IFN-α基因型与SLE风险显著相关。