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本文引用的文献

1
Opposing functions of IKKbeta during acute and chronic intestinal inflammation.IKKβ在急性和慢性肠道炎症中的相反作用。
Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):15058-63. doi: 10.1073/pnas.0808216105. Epub 2008 Sep 24.
2
Cancer-related inflammation.癌症相关炎症
Nature. 2008 Jul 24;454(7203):436-44. doi: 10.1038/nature07205.
3
An antiinflammatory role for IKKbeta through the inhibition of "classical" macrophage activation.IKKβ 通过抑制 “经典” 巨噬细胞活化发挥抗炎作用。
J Exp Med. 2008 Jun 9;205(6):1269-76. doi: 10.1084/jem.20080124. Epub 2008 May 19.
4
"Re-educating" tumor-associated macrophages by targeting NF-kappaB.通过靶向核因子-κB对肿瘤相关巨噬细胞进行“再教育”
J Exp Med. 2008 Jun 9;205(6):1261-8. doi: 10.1084/jem.20080108. Epub 2008 May 19.
5
NF-kappaB is a negative regulator of IL-1beta secretion as revealed by genetic and pharmacological inhibition of IKKbeta.如通过IKKβ的基因和药理学抑制所揭示的,核因子κB是白细胞介素-1β分泌的负调节因子。
Cell. 2007 Sep 7;130(5):918-31. doi: 10.1016/j.cell.2007.07.009.
6
Cytokine inhibitors in rheumatoid arthritis and other autoimmune diseases.类风湿关节炎及其他自身免疫性疾病中的细胞因子抑制剂
Curr Opin Pharmacol. 2007 Aug;7(4):412-7. doi: 10.1016/j.coph.2007.06.001. Epub 2007 Jul 12.
7
Control of specificity and magnitude of NF-kappa B and STAT1-mediated gene activation through PIASy and PIAS1 cooperation.通过PIASy和PIAS1协同作用控制NF-κB和STAT1介导的基因激活的特异性和强度。
Proc Natl Acad Sci U S A. 2007 Jul 10;104(28):11643-8. doi: 10.1073/pnas.0701877104. Epub 2007 Jul 2.
8
Proinflammatory stimuli induce IKKalpha-mediated phosphorylation of PIAS1 to restrict inflammation and immunity.促炎刺激诱导IKKα介导的PIAS1磷酸化,以限制炎症和免疫。
Cell. 2007 Jun 1;129(5):903-14. doi: 10.1016/j.cell.2007.03.056.
9
Chronic inflammation: a failure of resolution?慢性炎症:是消退失败吗?
Int J Exp Pathol. 2007 Apr;88(2):85-94. doi: 10.1111/j.1365-2613.2006.00507.x.
10
IKKalpha in the regulation of inflammation and adaptive immunity.IKKα在炎症调节和适应性免疫中的作用。
Biochem Soc Trans. 2007 Apr;35(Pt 2):270-2. doi: 10.1042/BST0350270.

炎症中的核因子 NF-κB 通路。

The nuclear factor NF-kappaB pathway in inflammation.

机构信息

Inflammation Biology Group, Centre d'Immunologie Marseille-Luminy, Parc Scientifique de Luminy, Case 906, 13288 Marseille, France.

出版信息

Cold Spring Harb Perspect Biol. 2009 Dec;1(6):a001651. doi: 10.1101/cshperspect.a001651. Epub 2009 Oct 7.

DOI:10.1101/cshperspect.a001651
PMID:20457564
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2882124/
Abstract

The nuclear factor NF-kappaB pathway has long been considered a prototypical proinflammatory signaling pathway, largely based on the role of NF-kappaB in the expression of proinflammatory genes including cytokines, chemokines, and adhesion molecules. In this article, we describe how genetic evidence in mice has revealed complex roles for the NF-kappaB in inflammation that suggest both pro- and anti-inflammatory roles for this pathway. NF-kappaB has long been considered the "holy grail" as a target for new anti-inflammatory drugs; however, these recent studies suggest this pathway may prove a difficult target in the treatment of chronic disease. In this article, we discuss the role of NF-kappaB in inflammation in light of these recent studies.

摘要

核因子 NF-κB 途径长期以来一直被认为是典型的促炎信号通路,这主要基于 NF-κB 在促炎基因(包括细胞因子、趋化因子和黏附分子)表达中的作用。在本文中,我们将描述小鼠中的遗传证据如何揭示了 NF-κB 在炎症中的复杂作用,这表明该途径既具有促炎作用,也具有抗炎作用。NF-κB 长期以来一直被视为新的抗炎药物的“圣杯”靶点;然而,这些最近的研究表明,该途径在治疗慢性疾病时可能是一个难以攻克的靶点。在本文中,我们将根据这些最近的研究讨论 NF-κB 在炎症中的作用。