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Cytokine Growth Factor Rev. 2006 Dec;17(6):451-61. Epub 2006 Oct 12.

Interleukin-6 trans-signaling in inflammatory bowel disease.

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1
Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, Asahi-machi 67, Kurume 830-0011, Japan. ibd@med.kurume-u.ac.jp

Abstract

The pathogenesis of inflammatory bowel disease (IBD) is complex, involving a wide range of molecules including cytokines. Recent investigations support the important role of an interleukin-6 (IL-6) signaling pathway in the development of IBD. However, the molecular mechanisms of this pathway in the intestine remain incompletely understood. The circulating and intestinal levels of IL-6 as well as soluble IL-6 receptor (sIL-6R) are increased in patients with IBD. It is remarkable that the mucosal T cells of IBD patients are extremely resistant to apoptosis and that a large fraction of these cells express membrane-bound gp130 but not IL-6R. The accumulated evidence strongly supports the hypothesis that the development and perpetuation of IBD relies on the increased formation of IL-6/sIL-6R complexes interacting with membrane-bound gp130 on T cells via trans-signaling. These studies suggest that IL-6 trans-signaling may play a role in the development of IBD; they therefore imply the possibility of a selective therapeutic strategy to target this signaling.

PMID:
17045835
DOI:
10.1016/j.cytogfr.2006.09.003
[Indexed for MEDLINE]
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