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系统性红斑狼疮(SLE)是一种复杂的多系统的自身免疫病。大量研究发现Toll样受体(TLRs)参与SLE的发病,MyD88(系大多数TLR信号一个关键的转接分子)缺陷狼疮鼠不发生自身免疫病。当TLR3、TLR7和TLR9信号在狼疮鼠同时被删除,其抗核抗体和狼疮症状都明显减轻。TLR7主要识别多种小分子抗病毒化合物如imiquimod,以及病毒单链RNA也参与狼疮活动,与SLE器官功能损害存在相关性。缺乏TLR7的MRL/lpr小鼠不产生抗RNA相关抗原的自身抗体,淋巴细胞活化降低,血清IgG水平下降,狼疮症状有所改善。因此,研究TLRs信号通路在狼疮疾病中的作用机理,有望对防治狼疮疾病提供新的靶标。
SLE is a complex, multisystem autoimmune disease. Numerous studies have found that Toll-like receptors (TLRs) are involved in the pathogenesis of SLE and that MyD88 (a key adapter molecule of most TLRs) does not develop autoimmune diseases in mice with lupus. When the TLR3, TLR7 and TLR9 signals were simultaneously deleted in lupus mice, their antinuclear antibodies and lupus symptoms were significantly reduced. TLR7 mainly recognizes a variety of small molecule antiviral compounds such as imiquimod, and viral single-stranded RNA is also involved in lupus activity, which is associated with impaired SLE organ function. MRL / lpr mice lacking TLR7 did not produce autoantibodies against RNA-associated antigens, decreased lymphocyte activation, decreased serum IgG levels, and improved lupus symptoms. Therefore, the study of TLRs signaling pathway in the pathogenesis of lupus disease, is expected to provide a new target for the prevention and treatment of lupus disease.