Impact of interleukin-6 classic- and trans-signaling on liver damage and regeneration

被引：69
|
作者：
Drucker, Claudia [1 ]
Gewiese, Jessica [1 ]
Malchow, Sven [1 ]
Scheller, Juergen [1 ]
Rose-John, Stefan [1 ]
机构：
[1] Univ Kiel, Inst Biochem, D-24098 Kiel, Germany
来源：
JOURNAL OF AUTOIMMUNITY | 2010年 / 34卷 / 01期
关键词：
Cancer; Inflammation; Interleukin-6; Liver; Trans-signaling; SOLUBLE IL-6 RECEPTOR; CELL-MEDIATED HEPATITIS; NECROSIS-FACTOR-ALPHA; A-INDUCED HEPATITIS; CARBON-TETRACHLORIDE; IN-VIVO; T-CELLS; DESIGNER CYTOKINE; OPPOSING ROLES; FUSION PROTEIN;
D O I：
10.1016/j.jaut.2009.08.003
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Interleukin-6 (IL-6) has been suggested to play a pivotal role in liver regeneration. IL-6 on target cells activates a receptor complex consisting of the IL-6 receptor (IL-6R) and the signal transducing receptor subunit gp130. Not all cells in the body express the IL-6R on the cell surface. IL-6 can signal via two different pathways: classical signaling via the membrane bound IL-6R and IL-6 trans-signaling via a naturally occurring soluble IL-6R (sIL-6R). This second pathway widens the scope of IL-6 signaling since also cells expressing no membrane bound IL-6R can be stimulated by the trans-signal pathway. Mimicking IL-6 trans-signaling via a designer molecule, Hyper-IL-6 has been shown to accelerate liver regeneration. Another designer molecule, sgp130Fc, specifically blocks IL-6 trans-signaling. Using these proteins we investigated the contribution of IL-6 classic- and trans-signaling in the liver. Here we review the role of IL-6 signaling in response to liver damage and during liver regeneration. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码：29 / 37
页数：9
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