Identification of the 80-kDa LPS-binding protein (LMP80) as decay-accelerating factor (DAF, CD55)

被引:36
作者
El-Samalouti, VT
Schletter, J
Chyla, I
Lentschat, A
Mamat, U
Brade, L
Flad, HD
Ulmer, AJ
Hamann, L
机构
[1] Res Ctr Borstel, Ctr Med & Biosci, D-23845 Borstel, Germany
[2] Gentherapeut Syst AG, Cardiogene, D-40699 Erkrath, Germany
来源
FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY | 1999年 / 23卷 / 03期
关键词
CD55; decay-accelerating factor; endotoxin; lipopolysaccharide; lipopolysaccharide-binding protein; LMP80;
D O I
10.1111/j.1574-695X.1999.tb01247.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The activation of immunocompetent cells by lipopolysaccharide (LPS) during severe Gram-negative infections is responsible for the pathophysiological reactions, possibly resulting in the clinical picture of sepsis. Monocytes recognize LPS mainly through the LPS receptor CD14, however, other cellular binding structures have been assumed to exist. In previous studies, we have described an 80-kDa LPS-binding membrane protein (LMP80), which is present on human monocytes as well as endothelial cells. Here we demonstrate that LMP80 is widely distributed and that it formes complexes together with LPS and sCD14. Furthermore, we report on the biochemical purification of LMP80 and its identification as decay-accelerating factor, CD55, by amino acid sequencing and cloning techniques. Our results imply a new feature of CD55 as a molecule which interacts with LPS/sCD14 complexes. However, the involvement of CD55 in LPS-induced signaling remains to be elucidated. (C) 1999 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:259 / 269
页数:11
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