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Epithelia: not just physical barriers.

作者信息

Ganz Tomas

机构信息

Department of Medicine, School of Medicine, University of California, Los Angeles, CA 90095, USA.

出版信息

Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3357-8. doi: 10.1073/pnas.072073199.

DOI:10.1073/pnas.072073199
PMID:11904396
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC122525/
Abstract
摘要

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本文引用的文献

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Lipid mediator-induced expression of bactericidal/ permeability-increasing protein (BPI) in human mucosal epithelia.脂质介质诱导人黏膜上皮细胞中杀菌/通透性增加蛋白（BPI）的表达。
Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3902-7. doi: 10.1073/pnas.052533799. Epub 2002 Mar 12.
2
Cutting edge: bacterial flagellin activates basolaterally expressed TLR5 to induce epithelial proinflammatory gene expression.前沿：细菌鞭毛蛋白激活基底外侧表达的TLR5以诱导上皮促炎基因表达。
J Immunol. 2001 Aug 15;167(4):1882-5. doi: 10.4049/jimmunol.167.4.1882.
3
Evidence for an innate immune response in the immature human intestine: toll-like receptors on fetal enterocytes.未成熟人类肠道中先天性免疫反应的证据：胎儿肠上皮细胞上的 Toll 样受体
Pediatr Res. 2001 Apr;49(4):589-93. doi: 10.1203/00006450-200104000-00023.
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Tlr4: central component of the sole mammalian LPS sensor.Tlr4：唯一的哺乳动物LPS传感器的核心组件。
Curr Opin Immunol. 2000 Feb;12(1):20-6. doi: 10.1016/s0952-7915(99)00046-1.
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Lipoxin and aspirin-triggered 15-epi-lipoxin cellular interactions anti-inflammatory lipid mediators.脂氧素和阿司匹林触发的15-表-脂氧素细胞相互作用抗炎脂质介质。
Clin Chem Lab Med. 1999 Mar;37(3):299-309. doi: 10.1515/CCLM.1999.052.
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Science. 1999 May 21;284(5418):1313-8. doi: 10.1126/science.284.5418.1313.
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Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene.C3H/HeJ和C57BL/10ScCr小鼠中LPS信号传导缺陷：Tlr4基因的突变
Science. 1998 Dec 11;282(5396):2085-8. doi: 10.1126/science.282.5396.2085.
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J Clin Invest. 1998 Apr 15;101(8):1633-42. doi: 10.1172/JCI1861.
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Nature. 1997 Jun 26;387(6636):861. doi: 10.1038/43088.
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Antibacterial proteins of granulocytes differ in interaction with endotoxin. Comparison of bactericidal/permeability-increasing protein, p15s, and defensins.粒细胞抗菌蛋白与内毒素的相互作用存在差异。杀菌/通透性增加蛋白、p15s和防御素的比较。
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