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TRAF1 regulates recruitment of lymphocytes and, to a lesser extent, neutrophils, myeloid dendritic cells and monocytes to the lung airways following lipopolysaccharide inhalation.TRAF1调节淋巴细胞的募集，并且在较小程度上，调节脂多糖吸入后中性粒细胞、髓样树突状细胞和单核细胞向肺气道的募集。
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本文引用的文献

1
Tumor necrosis factor receptor-associated factor (TRAF) 1 regulates CD40-induced TRAF2-mediated NF-kappaB activation.肿瘤坏死因子受体相关因子（TRAF）1调节CD40诱导的TRAF2介导的核因子κB激活。
J Biol Chem. 2004 Jan 2;279(1):677-85. doi: 10.1074/jbc.M310969200. Epub 2003 Oct 13.
2
Nuclear factor-kappa B plays a central role in tumour necrosis factor-mediated liver disease.核因子-κB在肿瘤坏死因子介导的肝脏疾病中起核心作用。
Biochem Pharmacol. 2003 Oct 15;66(8):1409-15. doi: 10.1016/s0006-2952(03)00491-x.
3
The future of GI and liver research: editorial perspectives. III. JNK/AP-1 regulation of hepatocyte death.胃肠与肝脏研究的未来：编辑观点。III. JNK/AP-1对肝细胞死亡的调控
Am J Physiol Gastrointest Liver Physiol. 2003 Jun;284(6):G875-9. doi: 10.1152/ajpgi.00549.2002.
4
Caspase-mediated cleavage converts the tumor necrosis factor (TNF) receptor-associated factor (TRAF)-1 from a selective modulator of TNF receptor signaling to a general inhibitor of NF-kappaB activation.半胱天冬酶介导的裂解将肿瘤坏死因子（TNF）受体相关因子（TRAF）-1从TNF受体信号传导的选择性调节剂转变为核因子κB激活的通用抑制剂。
J Biol Chem. 2003 Aug 1;278(31):29216-30. doi: 10.1074/jbc.M211090200. Epub 2003 Apr 22.
5
Protective role of Kupffer cells in acetaminophen-induced hepatic injury in mice.库普弗细胞在对乙酰氨基酚诱导的小鼠肝损伤中的保护作用。
Chem Res Toxicol. 2002 Dec;15(12):1504-13. doi: 10.1021/tx0255976.
6
Regulation of the subcellular localization of tumor necrosis factor receptor-associated factor (TRAF)2 by TRAF1 reveals mechanisms of TRAF2 signaling.肿瘤坏死因子受体相关因子1（TRAF1）对肿瘤坏死因子受体相关因子2（TRAF2）亚细胞定位的调控揭示了TRAF2信号传导机制。
J Exp Med. 2002 Oct 7;196(7):923-34. doi: 10.1084/jem.20020774.
7
CD40-mediated activation of NF-kappa B in airway epithelial cells.气道上皮细胞中CD40介导的核因子κB激活
J Biol Chem. 2002 Oct 4;277(40):37054-63. doi: 10.1074/jbc.M205778200. Epub 2002 Jul 16.
8
Apoptotic crosstalk of TNF receptors: TNF-R2-induces depletion of TRAF2 and IAP proteins and accelerates TNF-R1-dependent activation of caspase-8.肿瘤坏死因子受体的凋亡串扰：肿瘤坏死因子受体2诱导肿瘤坏死因子受体相关因子2和凋亡抑制蛋白的消耗，并加速肿瘤坏死因子受体1依赖性半胱天冬酶8的激活。
J Cell Sci. 2002 Jul 1;115(Pt 13):2757-70. doi: 10.1242/jcs.115.13.2757.
9
TRAF1 is a negative regulator of TNF signaling. enhanced TNF signaling in TRAF1-deficient mice.TRAF1是肿瘤坏死因子（TNF）信号传导的负调节因子。在缺乏TRAF1的小鼠中，TNF信号传导增强。
Immunity. 2001 Oct;15(4):647-57. doi: 10.1016/s1074-7613(01)00207-2.
10
The TNF-receptor-associated factor family: scaffold molecules for cytokine receptors, kinases and their regulators.肿瘤坏死因子受体相关因子家族：细胞因子受体、激酶及其调节因子的支架分子。
Cell Signal. 2001 Jun;13(6):389-400. doi: 10.1016/s0898-6568(01)00160-7.

在缺乏肿瘤坏死因子受体相关因子1基因表达的情况下，急性肿瘤坏死因子-α诱导的肝损伤。

Acute tumor necrosis factor-alpha-induced liver injury in the absence of tumor necrosis factor receptor-associated factor 1 gene expression.

作者信息

Pryhuber Gloria S, Huyck Heidie L, Roper Jason M, Cornejo Judith, O'Reilly Michael A, Pierce Robert H, Tsitsikov Erdyni N

机构信息

Department of Pediatrics, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

出版信息

Am J Pathol. 2005 Jun;166(6):1637-45. doi: 10.1016/s0002-9440(10)62474-1.

DOI:10.1016/s0002-9440(10)62474-1
PMID:15920149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1602417/
Abstract

Pulmonary and serum levels of tumor necrosis factor-alpha (TNF-alpha), are elevated in many lung diseases, causing local inflammation, fever, and multiorgan, including hepatic, dysfunction. Cellular responses to TNF-alpha are determined by recruitment of specific proteins to intracellular receptor signaling complexes. One of these proteins, TNF receptor-associated factor 1 (TRAF1), is highly regulated in pulmonary cells. To determine the effect of reduced pulmonary TRAF1 expression, TRAF1-null (-/-) and control, BALB/c (wild-type), mice were treated intratracheally, intraperitoneally, or intravenously, with TNF-alpha. Despite relatively mild lung injury, intratracheal TNF-alpha-treated TRAF1-/- mice exhibited marked liver injury with an approximate fivefold increase in serum liver enzyme levels as compared to wild-type mice. In addition, serum TNF-alpha levels were strikingly elevated in TRAF1-/- mice. Pretreatment with neutralizing anti-TNFRI antibody significantly reduced liver injury and serum TNF-alpha. Cells isolated by bronchoalveolar lavage from intratracheally treated TRAF1-/- mice produced more TNF-alpha than cells from treated wild-type mice, suggesting that lung cells contributed to elevated serum TNF-alpha. These studies suggest that TRAF1 provides negative feedback for TNF-alpha synthesis and limits TNFRI-mediated systemic effects of TNF-alpha originating in the lung.

摘要

在许多肺部疾病中，肿瘤坏死因子-α（TNF-α）的肺部和血清水平会升高，引发局部炎症、发热以及包括肝脏功能障碍在内的多器官功能障碍。细胞对TNF-α的反应取决于特定蛋白质向细胞内受体信号复合物的募集。其中一种蛋白质，即TNF受体相关因子1（TRAF1），在肺细胞中受到高度调控。为了确定肺部TRAF1表达降低的影响，将TRAF1基因敲除（-/-）小鼠和对照BALB/c（野生型）小鼠经气管内、腹腔内或静脉内给予TNF-α。尽管肺部损伤相对较轻，但与野生型小鼠相比，经气管内给予TNF-α处理的TRAF1-/-小鼠表现出明显的肝损伤，血清肝酶水平大约增加了五倍。此外，TRAF1-/-小鼠的血清TNF-α水平显著升高。用中和性抗TNFRI抗体预处理可显著减轻肝损伤和血清TNF-α水平。经气管内处理的TRAF1-/-小鼠支气管肺泡灌洗分离出的细胞比经处理的野生型小鼠的细胞产生更多的TNF-α，这表明肺细胞导致血清TNF-α水平升高。这些研究表明，TRAF1为TNF-α合成提供负反馈，并限制源自肺部的TNF-α的TNFRI介导的全身效应。