阐明重症哮喘。
Shedding LIGHT on severe asthma.
出版信息
Nat Med. 2011 May;17(5):547-8. doi: 10.1038/nm0511-547.
Abstract
Moderate to severe asthma is difficult to treat because recurring bouts of inflammation in the lungs induce fibrosis, which reduces lung elasticity, gas exchange and responses to conventional therapy. A recent study identifies the tumor necrosis factor family member LIGHT as an essential mediator of airway fibrosis in a mouse model of chronic asthma (pages 596–603).
摘要
中度至重度哮喘难以治疗，因为肺部反复发生的炎症会导致纤维化，从而降低肺弹性、气体交换和对常规治疗的反应。最近的一项研究确定肿瘤坏死因子家族成员 LIGHT 是慢性哮喘小鼠模型中气道纤维化的重要介质（第 596-603 页）。
相似文献
1
Shedding LIGHT on severe asthma.阐明重症哮喘。
Nat Med. 2011 May;17(5):547-8. doi: 10.1038/nm0511-547.
2
The tumor necrosis factor family member LIGHT is a target for asthmatic airway remodeling.肿瘤坏死因子家族成员 LIGHT 是哮喘气道重塑的靶点。
Nat Med. 2011 May;17(5):596-603. doi: 10.1038/nm.2356. Epub 2011 Apr 17.
3
Effect of tumor necrosis factor family member LIGHT (TNFSF14) on the activation of basophils and eosinophils interacting with bronchial epithelial cells.肿瘤坏死因子家族成员LIGHT（TNFSF14）对与支气管上皮细胞相互作用的嗜碱性粒细胞和嗜酸性粒细胞激活的影响。
Mediators Inflamm. 2014;2014:136463. doi: 10.1155/2014/136463. Epub 2014 Mar 25.
4
Chronic viral hepatitis and iron affect the plasma levels of LIGHT--a new member of the TNF superfamily in uraemic haemodialyzed patients.慢性病毒性肝炎和铁元素会影响尿毒症血液透析患者血浆中LIGHT的水平——LIGHT是肿瘤坏死因子超家族的一个新成员。
Cytokine. 2007 Sep;39(3):201-6. doi: 10.1016/j.cyto.2007.07.189. Epub 2007 Sep 10.
5
Tumor necrosis factor superfamily member LIGHT induces epithelial-mesenchymal transition in A549 human alveolar epithelial cells.肿瘤坏死因子超家族成员 LIGHT 诱导 A549 人肺泡上皮细胞发生上皮-间充质转化。
Biochem Biophys Res Commun. 2012 Nov 30;428(4):451-7. doi: 10.1016/j.bbrc.2012.10.097. Epub 2012 Nov 3.
6
IL-17E upregulates the expression of proinflammatory cytokines in lung fibroblasts.白细胞介素-17E上调肺成纤维细胞中促炎细胞因子的表达。
J Allergy Clin Immunol. 2006 Mar;117(3):590-6. doi: 10.1016/j.jaci.2005.10.025. Epub 2006 Feb 8.
7
Polymorphic variants of LIGHT (TNF superfamily-14) alter receptor avidity and bioavailability.LIGHT（TNF 超家族-14）的多态变体改变了受体的亲合力和生物利用度。
J Immunol. 2010 Aug 1;185(3):1949-58. doi: 10.4049/jimmunol.1001159. Epub 2010 Jun 30.
8
Lymphotoxin-alpha 1 beta 2 and LIGHT induce classical and noncanonical NF-kappa B-dependent proinflammatory gene expression in vascular endothelial cells.淋巴毒素-α1β2和LIGHT可诱导血管内皮细胞中经典和非经典的核因子κB依赖性促炎基因表达。
J Immunol. 2008 Mar 1;180(5):3467-77. doi: 10.4049/jimmunol.180.5.3467.
9
Transforming growth factor-beta1 suppresses airway hyperresponsiveness in allergic airway disease.转化生长因子-β1抑制变应性气道疾病中的气道高反应性。
Am J Respir Crit Care Med. 2007 Nov 15;176(10):974-82. doi: 10.1164/rccm.200702-334OC. Epub 2007 Aug 29.
10
Interleukin-13's key role in asthma shown.白细胞介素-13在哮喘中的关键作用已得到证实。
Science. 1998 Dec 18;282(5397):2168. doi: 10.1126/science.282.5397.2168a.
引用本文的文献
1
Increased LIGHT leading to sFlt-1 elevation underlies the pathogenic link between hydatidiform mole and preeclampsia.LIGHT 的增加导致 sFlt-1 的升高，这是葡萄胎和子痫前期之间发病机制的联系。
Sci Rep. 2019 Jul 12;9(1):10107. doi: 10.1038/s41598-019-46660-4.
2
The Role of TNF Family Molecules Light in Cellular Interaction Between Airway Smooth Muscle Cells and T Cells During Chronic Allergic Inflammation.TNF 家族分子在慢性变应性炎症中气道平滑肌细胞与 T 细胞间细胞相互作用中的作用。
Inflammation. 2018 Jun;41(3):1021-1031. doi: 10.1007/s10753-018-0755-1.
3
Effect of tumor necrosis factor family member LIGHT (TNFSF14) on the activation of basophils and eosinophils interacting with bronchial epithelial cells.肿瘤坏死因子家族成员LIGHT（TNFSF14）对与支气管上皮细胞相互作用的嗜碱性粒细胞和嗜酸性粒细胞激活的影响。
Mediators Inflamm. 2014;2014:136463. doi: 10.1155/2014/136463. Epub 2014 Mar 25.
4
Excess LIGHT contributes to placental impairment, increased secretion of vasoactive factors, hypertension, and proteinuria in preeclampsia.过量的 LIGHT 可导致胎盘损伤、血管活性因子分泌增加、高血压和子痫前期的蛋白尿。
Hypertension. 2014 Mar;63(3):595-606. doi: 10.1161/HYPERTENSIONAHA.113.02458. Epub 2013 Dec 9.
本文引用的文献
1
The tumor necrosis factor family member LIGHT is a target for asthmatic airway remodeling.肿瘤坏死因子家族成员 LIGHT 是哮喘气道重塑的靶点。
Nat Med. 2011 May;17(5):596-603. doi: 10.1038/nm.2356. Epub 2011 Apr 17.
2
T-helper type 2-driven inflammation defines major subphenotypes of asthma.2型辅助性T细胞驱动的炎症反应定义了哮喘的主要亚表型。
Am J Respir Crit Care Med. 2009 Sep 1;180(5):388-95. doi: 10.1164/rccm.200903-0392OC. Epub 2009 May 29.
3
Pulmonary fibrosis: pathogenesis, etiology and regulation.肺纤维化：发病机制、病因及调控
Mucosal Immunol. 2009 Mar;2(2):103-21. doi: 10.1038/mi.2008.85. Epub 2009 Jan 7.
4
Immunology of asthma and chronic obstructive pulmonary disease.哮喘与慢性阻塞性肺疾病的免疫学
Nat Rev Immunol. 2008 Mar;8(3):183-92. doi: 10.1038/nri2254. Epub 2008 Feb 15.
5
National surveillance for asthma--United States, 1980-2004.美国1980 - 2004年哮喘病国家监测
MMWR Surveill Summ. 2007 Oct 19;56(8):1-54.
6
Evidence of a role of tumor necrosis factor alpha in refractory asthma.肿瘤坏死因子α在难治性哮喘中作用的证据。
N Engl J Med. 2006 Feb 16;354(7):697-708. doi: 10.1056/NEJMoa050580.
7
Network communications: lymphotoxins, LIGHT, and TNF.网络通讯：淋巴毒素、LIGHT和肿瘤坏死因子。
Annu Rev Immunol. 2005;23:787-819. doi: 10.1146/annurev.immunol.23.021704.115719.
8
Targeted disruption of LIGHT causes defects in costimulatory T cell activation and reveals cooperation with lymphotoxin beta in mesenteric lymph node genesis.LIGHT的靶向破坏导致共刺激T细胞活化缺陷，并揭示其在肠系膜淋巴结发生过程中与淋巴毒素β的协同作用。
J Exp Med. 2002 Jun 17;195(12):1613-24. doi: 10.1084/jem.20020215.
9
The regulation of T cell homeostasis and autoimmunity by T cell-derived LIGHT.T细胞来源的LIGHT对T细胞稳态和自身免疫的调节
J Clin Invest. 2001 Dec;108(12):1771-80. doi: 10.1172/JCI13827.
10
Constitutive expression of LIGHT on T cells leads to lymphocyte activation, inflammation, and tissue destruction.T细胞上LIGHT的组成型表达会导致淋巴细胞活化、炎症和组织破坏。
J Immunol. 2001 Dec 1;167(11):6330-7. doi: 10.4049/jimmunol.167.11.6330.
Zotero 插件