Induction of autoimmunity by pristane and other naturally occurring hydrocarbons.
Induction of autoimmunity by pristane and other naturally occurring hydrocarbons.
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DOI：
10.1016/j.it.2009.06.003
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发表时间：
2009-09
影响因子：
16.8
通讯作者：
Lu L
中科院分区：
文献类型：
--
作者：
Reeves WH;Lee PY;Weinstein JS;Satoh M;Lu L
四甲基十五烷(TMPD，或俗称Pristane)诱导的狼疮是系统性红斑狼疮(SLE)的小鼠模型。肾脏疾病和自身抗体的产生严格依赖于通过干扰素-I受体传递的信号。干扰素-I的主要来源是未成熟的单核细胞，其表面标记Ly6C水平较高。干扰素的产生完全是通过TLR7和接头蛋白MyD88的信号来调节的。很可能是内源性TLR7配体，如小核核糖核蛋白复合体的成分，参与了引发疾病的过程。狼疮自身抗体产生于异位淋巴组织对TMPD的反应。这一模型非常适合于研究干扰素-I分泌失调与人类系统性红斑狼疮的发病机制之间的联系。与TMPD-狼疮一样，人类系统性红斑狼疮与高水平的干扰素-I有关。
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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DOI：
10.1084/jem.20021553
发表时间：
2003-03-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Bennett L;Palucka AK;Arce E;Cantrell V;Borvak J;Banchereau J;Pascual V
通讯作者：
Pascual V
影响因子：
19.6
作者：
Calvani, N;Satoh, M;Richards, HB
通讯作者：
Richards, HB
影响因子：
3.3
作者：
CRUICKSHANK, B
通讯作者：
CRUICKSHANK, B
影响因子：
3.5
作者：
DINCSOY, HP;WEESNER, RE;MACGEE, J
通讯作者：
MACGEE, J
影响因子：
5.4
作者：
GAUSE, A;GUNDLACH, K;PFREUNDSCHUH, M
通讯作者：
PFREUNDSCHUH, M