免疫学
TLR7型
自身免疫
系统性红斑狼疮
自身抗体
正庚烷
Ⅰ型干扰素
干扰素
发病机制
核糖核蛋白
自身免疫性疾病
生物
医学
疾病
化学
抗体
Toll样受体
免疫系统
核糖核酸
内科学
基因
先天免疫系统
生物化学
碳氢化合物
有机化学
作者
Westley H. Reeves,Pui Y. Lee,Jason S. Weinstein,Minoru Satoh,Li Lü
标识
DOI:10.1016/j.it.2009.06.003
摘要
Tetramethylpentadecane (TMPD, or commonly known as pristane)-induced lupus is a murine model of systemic lupus erythematosus (SLE). Renal disease and autoantibody production strictly depend on signaling through the interferon (IFN)-I receptor. The major source of IFN-I is immature monocytes bearing high levels of the surface marker Ly6C. Interferon production is mediated exclusively by signaling through TLR7 and the adapter protein MyD88. It is likely that endogenous TLR7 ligands such as components of small nuclear ribonucleoprotein complexes are involved in triggering disease. Lupus autoantibodies are produced in ectopic lymphoid tissue developing in response to TMPD. This model is well suited for examining links between dysregulated IFN-I production and the pathogenesis of human SLE, which like TMPD-lupus, is associated with high levels of IFN-I.
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