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本文引用的文献

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Aryl hydrocarbon receptor-induced signals up-regulate IL-22 production and inhibit inflammation in the gastrointestinal tract.芳基烃受体诱导的信号上调白细胞介素 22 的产生并抑制胃肠道炎症。
Gastroenterology. 2011 Jul;141(1):237-48, 248.e1. doi: 10.1053/j.gastro.2011.04.007. Epub 2011 Apr 16.
2
Distinct roles of IL-22 in human psoriasis and inflammatory bowel disease.IL-22 在人类银屑病和炎症性肠病中的不同作用。
Cytokine Growth Factor Rev. 2010 Dec;21(6):435-41. doi: 10.1016/j.cytogfr.2010.10.007. Epub 2010 Nov 23.
3
The London Position Statement of the World Congress of Gastroenterology on Biological Therapy for IBD with the European Crohn's and Colitis Organization: when to start, when to stop, which drug to choose, and how to predict response?世界胃肠病学大会与欧洲克罗恩病和结肠炎组织关于 IBD 的生物治疗的伦敦立场声明：何时开始，何时停止，选择哪种药物，以及如何预测应答？
Am J Gastroenterol. 2011 Feb;106(2):199-212; quiz 213. doi: 10.1038/ajg.2010.392. Epub 2010 Nov 2.
4
Inflammatory bowel disease.炎症性肠病。
Annu Rev Immunol. 2010;28:573-621. doi: 10.1146/annurev-immunol-030409-101225.
5
Tumor necrosis factor alpha blockade exacerbates murine psoriasis-like disease by enhancing Th17 function and decreasing expansion of Treg cells.肿瘤坏死因子α阻断通过增强Th17功能和减少调节性T细胞的扩增来加重小鼠银屑病样疾病。
Arthritis Rheum. 2010 Feb;62(2):430-40. doi: 10.1002/art.27203.
6
Efficacy and safety of certolizumab pegol induction therapy in an unselected Crohn's disease population: results of the FACTS survey.在未选择的克罗恩病人群中，培塞丽珠单药诱导治疗的疗效和安全性：FACTS 调查结果。
Inflamm Bowel Dis. 2010 Jun;16(6):933-8. doi: 10.1002/ibd.21127.
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Randomized, double-blind, placebo-controlled trial of the oral interleukin-12/23 inhibitor apilimod mesylate for treatment of active Crohn's disease.随机、双盲、安慰剂对照试验评估甲磺酸阿巴西普治疗活动期克罗恩病的疗效。
Inflamm Bowel Dis. 2010 Jul;16(7):1209-18. doi: 10.1002/ibd.21159.
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Inflammatory bowel disease and mutations affecting the interleukin-10 receptor.炎症性肠病与影响白细胞介素-10受体的突变
N Engl J Med. 2009 Nov 19;361(21):2033-45. doi: 10.1056/NEJMoa0907206. Epub 2009 Nov 4.
9
Fontolizumab in moderate to severe Crohn's disease: a phase 2, randomized, double-blind, placebo-controlled, multiple-dose study.FONTOLIZUMAB 在中重度克罗恩病中的应用：一项 2 期、随机、双盲、安慰剂对照、多剂量研究。
Inflamm Bowel Dis. 2010 Feb;16(2):233-42. doi: 10.1002/ibd.21038.
10
Crohn's disease: Th1, Th17 or both? The change of a paradigm: new immunological and genetic insights implicate Th17 cells in the pathogenesis of Crohn's disease.克罗恩病：是Th1、Th17，还是两者兼有？范式的转变：新的免疫学和遗传学见解表明Th17细胞参与克罗恩病的发病机制。
Gut. 2009 Aug;58(8):1152-67. doi: 10.1136/gut.2008.163667.

细胞因子靶向治疗炎症性肠病中炎症信号的阻断。

Disruption of inflammatory signals by cytokine-targeted therapies for inflammatory bowel diseases.

机构信息

Unit of Gastroenterology 2, Fondazione IRCCS Ca' Granda - Ospedale Maggiore Policlinico, Milan, Italy.

出版信息

Br J Pharmacol. 2012 Feb;165(4):820-8. doi: 10.1111/j.1476-5381.2011.01614.x.

DOI:10.1111/j.1476-5381.2011.01614.x
PMID:21806600
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3312480/
Abstract

Gut inflammation occurring in patients with inflammatory bowel diseases (IBD) is associated with an excessive immune response that is directed against constituents of the normal bacterial flora and results in the production of large amounts of inflammatory cytokines. Anti-cytokine compounds, such as the neutralizing TNF antibodies, have been employed with clinical success in patients with IBD. However, nearly half of IBD patients are refractory to such treatments, response can wane with time, and anti-TNF treatment can associate with severe side effects and/or development/exacerbation of extra-intestinal immune-mediated pathologies. These observations, and the demonstration that, in IBD, the pathological process is also characterized by defects in the production and/or activity of counter-regulatory cytokines, have boosted further studies aimed at delineating novel strategies to combat the IBD-associated tissue-damaging immune response.

摘要

肠道炎症发生在炎症性肠病（IBD）患者中，与针对正常细菌菌群成分的过度免疫反应有关，导致大量炎症细胞因子的产生。抗细胞因子化合物，如中和 TNF 的抗体，在 IBD 患者中已成功应用于临床。然而，近一半的 IBD 患者对此类治疗有抗性，随着时间的推移，反应可能会减弱，抗 TNF 治疗可能会与严重的副作用和/或肠道外免疫介导的病理的发展/恶化相关。这些观察结果，以及在 IBD 中，病理过程还表现为产生和/或调节细胞因子的活性缺陷的证明，促使进一步研究旨在制定新的策略来对抗与 IBD 相关的组织损伤性免疫反应。