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核因子κB在肠道免疫和炎症反应中的作用。

Role of NF-kappaB in immune and inflammatory responses in the gut.

作者信息

Neurath M F, Becker C, Barbulescu K

机构信息

Laboratory of Immunology, I. Medical Clinic, University of Mainz, Langenbeckstrasse, 55101 Mainz, Germany.

出版信息

Gut. 1998 Dec;43(6):856-60. doi: 10.1136/gut.43.6.856.

DOI:10.1136/gut.43.6.856
PMID:9824616
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1727350/
Abstract

NF-kappaB is a pleiotropic transcription factor with key functions in the intestinal immune system. NF-kappaB family members control transcriptional activity of various promoters of proinflammatory cytokines, cell surface receptors, transcription factors, and adhesion molecules that are involved in intestinal inflammation. The perpetuated activation of NF-kappaB in patients with active inflammatory bowel disease suggests that regulation of NF-kappaB activity is a very attractive target for therapeutic intervention. Such strategies include antioxidants, proteasome inhibitors, inhibition of NF-kappaB by adenoviral I kappaB alpha expression vectors, and antisense DNA targeting of NF-kappaB. These approaches will hopefully permit the design of new treatment strategies for chronic intestinal inflammation.

摘要

核因子-κB是一种多效性转录因子,在肠道免疫系统中发挥关键作用。核因子-κB家族成员控制着参与肠道炎症的多种促炎细胞因子、细胞表面受体、转录因子和黏附分子启动子的转录活性。在活动性炎症性肠病患者中,核因子-κB的持续激活表明,调节核因子-κB活性是一个极具吸引力的治疗干预靶点。此类策略包括抗氧化剂、蛋白酶体抑制剂、通过腺病毒IκBα表达载体抑制核因子-κB,以及针对核因子-κB的反义DNA。这些方法有望为慢性肠道炎症设计出新的治疗策略。

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本文引用的文献

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Mediation by NF-kappa B of cytokine induced expression of intercellular adhesion molecule 1 (ICAM-1) in an intestinal epithelial cell line, a process blocked by proteasome inhibitors.细胞因子诱导肠上皮细胞系中细胞间黏附分子1(ICAM-1)表达过程中NF-κB的介导作用,该过程被蛋白酶体抑制剂阻断。
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Nature. 1997 Feb 6;385(6616):540-4. doi: 10.1038/385540a0.
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Mol Cell Biol. 1996 Nov;16(11):6363-71. doi: 10.1128/MCB.16.11.6363.