Inflammatory chemokine expression via Toll-like receptor 3 signaling in normal human mesangial cells.
Inflammatory chemokine expression via Toll-like receptor 3 signaling in normal human mesangial cells.
复制标题
DOI：
10.1155/2013/984708
复制
发表时间：
2013
影响因子：
--
通讯作者：
Imaizumi T
中科院分区：
文献类型：
--
作者：
Tanaka H;Imaizumi T
先天性和适应性免疫系统已被报道在肾小球疾病的发病机制中发挥重要作用。由于病毒感染可能引发炎症性肾脏疾病的发展或先前存在的肾脏疾病的恶化，最近的研究集中在toll样受体（TLRs）及其信号通路在肾小球细胞炎症过程中的参与。病毒双链RNA （dsRNA）不仅可以激活位于细胞内核体的TLR3，还可以激活位于细胞质内的视黄酸诱导基因i - (RIG-I-)样解旋酶受体。rig - 1和黑色素瘤分化相关基因5 （MDA5）是细胞质中RNA解旋酶家族的成员，都是病原体识别受体。tlr的激活及其下游免疫应答既可由感染性病原体诱导，也可由内源性配体等非感染性刺激诱导，这一机制可能参与自身免疫性肾病的发病机制。然而，关于TLR3、MDA5和rig - 1在自身免疫性肾小球疾病中的相互作用的数据很少。我们最近利用培养的正常人系膜细胞（MCs）进行实验研究，发现MCs中tlr3介导的新型信号通路可能参与肾小球疾病的发病机制。在本文中，我们总结了我们最近的发现。
The innate and adaptive immune systems have been reported to play an important role in the pathogenesis of glomerular diseases. Since viral infections may trigger the development of inflammatory renal disease or the worsening of preexisting renal disease, recent studies have focused on the involvement of toll-like receptors (TLRs) and their signaling pathways in the inflammatory processes of glomerular cells. Viral double-stranded RNA (dsRNA) can activate not only TLR3 located within intracellular endosomes but also retinoic-acid-inducible-gene-I- (RIG-I-) like helicase receptors located within the cytosol. RIG-I and melanoma differentiation-associated gene 5 (MDA5) are members of the RNA helicase family in the cytosol, and both act as pathogen recognition receptors. The activation of TLRs and their downstream immune responses can be induced by both infectious pathogens and noninfectious stimuli such as endogenous ligands, and this mechanism may be involved in the pathogenesis of autoimmune renal diseases. However, there are few data on the interaction between TLR3, MDA5, and RIG-I in autoimmune glomerular diseases. Based on our recent experimental studies using cultured normal human mesangial cells (MCs), we found that novel TLR3-mediated signaling pathways in MCs may be involved in the pathogenesis of glomerular diseases. In the present paper, we summarize our recent findings.
登录
查看更多内容
影响因子：
3.4
作者：
Migliorini, Adriana;Ebid, Rainer;Anders, Hans-Joachim
通讯作者：
Anders, Hans-Joachim
影响因子：
6
作者：
Fluer, Katharina;Allam, Ramanjaneyulu;Anders, Hans-Joachim
通讯作者：
Anders, Hans-Joachim
影响因子：
3
作者：
Tsugawa, Koji;Oki, Eishin;Tanaka, Hiroshi
通讯作者：
Tanaka, Hiroshi
影响因子：
6.1
作者：
Haegele, Holger;Allam, Ramanjaneyulu;Anders, Hans-Joachim
通讯作者：
Anders, Hans-Joachim
影响因子：
6.1
作者：
Patole, Prashant S.;Pawar, Rahul D.;Anders, Hans-Joachim
通讯作者：
Anders, Hans-Joachim