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

页码：29 / 37

页数：9

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