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.
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DOI:
10.3389/fimmu.2018.02023
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发表时间:
2018
影响因子:
7.3
通讯作者:
Sacks S
Sacks S
中科院分区:
医学2区
文献类型:
--
作者:
Nauser CL;Howard MC;Fanelli G;Farrar CA;Sacks S

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补体系统是先天免疫系统的动态子集,在宿主防御、清除免疫复合物和细胞碎片以及引发适应性免疫应答中发挥作用。在过去的40年里,我们对补体系统的理解已经从确定其存在并认识到其在血液中的作用发展到现在专注于了解局部补体合成在健康和疾病中的作用。特别是,发现补体的局部合成参与介导缺血性损伤,包括移植后。最近关于阐明肾组织中局部补体合成和活化的触发因素的工作已经导致了以下发现:胶原凝集素-11(CL-11)在缺血应激部位(即在近端肾小管上皮细胞的表面)与L-岩藻糖接合。目前尚不清楚的是参与CL-11结合和随后的补体激活的损伤相关配体的精确结构。在本文中,我们将讨论我们关于CL-11作为一种完整的基于组织的模式识别分子的作用的假设,我们假设CL-11在补体介导的缺血性损伤中具有显着的贡献作用。
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.
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