Collectin-11 (CL-11) Is a Major Sentinel at Epithelial Surfaces and Key Pattern Recognition Molecule in Complement-Mediated Ischaemic Injury.
Collectin-11 (CL-11) Is a Major Sentinel at Epithelial Surfaces and Key Pattern Recognition Molecule in Complement-Mediated Ischaemic Injury.
复制标题
DOI:
10.3389/fimmu.2018.02023
复制
发表时间:
2018
影响因子:
7.3
通讯作者:
Sacks S
中科院分区:
文献类型:
--
作者:
Nauser CL;Howard MC;Fanelli G;Farrar CA;Sacks S
The complement system is a dynamic subset of the innate immune system, playing roles in host defense, clearance of immune complexes and cell debris, and priming the adaptive immune response. Over the last 40 years our understanding of the complement system has evolved from identifying its presence and recognizing its role in the blood to now focusing on understanding the role of local complement synthesis in health and disease. In particular, the local synthesis of complement was found to have an involvement in mediating ischaemic injury, including following transplantation. Recent work on elucidating the triggers of local complement synthesis and activation in renal tissue have led to the finding that Collectin-11 (CL-11) engages with L-fucose at the site of ischaemic stress, namely at the surface of the proximal tubular epithelial cells. What remains unknown is the precise structure of the damage-associated ligand that participates in CL-11 binding and subsequent complement activation. In this article, we will discuss our hypothesis regarding the role of CL-11 as an integral tissue-based pattern recognition molecule which we postulate has a significant contributory role in complement-mediated ischaemic injury.
登录
查看更多内容
影响因子:
5.4
作者:
ANDREWS, PA;FINN, JE;SACKS, SH
通讯作者:
SACKS, SH
影响因子:
9
作者:
Howard M;Farrar CA;Sacks SH
通讯作者:
Sacks SH
影响因子:
4.6
作者:
Fanelli G;Gonzalez-Cordero A;Gardner PJ;Peng Q;Fernando M;Kloc M;Farrar CA;Naeem A;Garred P;Ali RR;Sacks SH
通讯作者:
Sacks SH
影响因子:
4.4
作者:
Henriksen, Maiken L.;Brandt, Jette;Hansen, Soren
通讯作者:
Hansen, Soren
影响因子:
6.1
作者:
David, S;Biancone, L;Camussi, G
通讯作者:
Camussi, G