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TLR-induced activation of Btk -- role for endosomal MHC class II molecules revealed.

作者信息

Ní Gabhann Joan, Jefferies Caroline A

机构信息

Molecular and Cellular Therapeutics and RSCI Research Institute, Royal College of Surgeons in Ireland, Dublin, Ireland.

出版信息

Cell Res. 2011 Jul;21(7):998-1001. doi: 10.1038/cr.2011.88. Epub 2011 May 24.

DOI:10.1038/cr.2011.88
PMID:21606951
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3193487/
Abstract
摘要

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本文引用的文献

1
Intracellular MHC class II molecules promote TLR-triggered innate immune responses by maintaining activation of the kinase Btk.细胞内 MHC Ⅱ类分子通过维持激酶 Btk 的激活来促进 TLR 触发的固有免疫反应。
Nat Immunol. 2011 May;12(5):416-24. doi: 10.1038/ni.2015. Epub 2011 Mar 27.
2
Activation of MyD88 signaling upon staphylococcal enterotoxin binding to MHC class II molecules.金黄色葡萄球菌肠毒素与 MHC Ⅱ类分子结合后 MyD88 信号的激活。
PLoS One. 2011 Jan 20;6(1):e15985. doi: 10.1371/journal.pone.0015985.
3
Dendritic cell activation prevents MHC class II ubiquitination and promotes MHC class II survival regardless of the activation stimulus.树突状细胞的激活可防止 MHC Ⅱ类泛素化,并促进 MHC Ⅱ类的存活,而与激活刺激物无关。
J Biol Chem. 2010 Dec 31;285(53):41749-54. doi: 10.1074/jbc.M110.157586. Epub 2010 Nov 3.
4
TLR signaling and effector functions are intact in XLA neutrophils.XLA 中性粒细胞的 TLR 信号转导和效应功能完整。
Clin Immunol. 2010 Oct;137(1):74-80. doi: 10.1016/j.clim.2010.06.011. Epub 2010 Jul 14.
5
MHC class II molecules enhance Toll-like receptor mediated innate immune responses.MHC Ⅱ类分子增强 Toll 样受体介导的固有免疫应答。
PLoS One. 2010 Jan 20;5(1):e8808. doi: 10.1371/journal.pone.0008808.
6
Augmented TLR9-induced Btk activation in PIR-B-deficient B-1 cells provokes excessive autoantibody production and autoimmunity.在缺乏PIR-B的B-1细胞中,增强的TLR9诱导的Btk激活会引发过量自身抗体产生和自身免疫。
J Exp Med. 2009 Aug 31;206(9):1971-82. doi: 10.1084/jem.20082392. Epub 2009 Aug 17.
7
Signaling by Toll-like receptors 8 and 9 requires Bruton's tyrosine kinase.Toll样受体8和9的信号传导需要布鲁顿酪氨酸激酶。
J Biol Chem. 2007 Dec 21;282(51):36953-60. doi: 10.1074/jbc.M707682200. Epub 2007 Oct 11.
8
Bruton's tyrosine kinase is required for TLR2 and TLR4-induced TNF, but not IL-6, production.布鲁顿酪氨酸激酶是Toll样受体2(TLR2)和Toll样受体4(TLR4)诱导肿瘤坏死因子(TNF)产生所必需的,但不是白细胞介素-6(IL-6)产生所必需的。
J Immunol. 2006 Mar 15;176(6):3635-41. doi: 10.4049/jimmunol.176.6.3635.
9
Bruton's tyrosine kinase is involved in p65-mediated transactivation and phosphorylation of p65 on serine 536 during NFkappaB activation by lipopolysaccharide.布鲁顿酪氨酸激酶参与脂多糖激活核因子κB过程中p65介导的反式激活以及p65丝氨酸536位点的磷酸化。
J Biol Chem. 2005 Jun 24;280(25):23496-501. doi: 10.1074/jbc.C500053200. Epub 2005 Apr 22.
10
Toll-like receptor signalling.Toll样受体信号传导
Nat Rev Immunol. 2004 Jul;4(7):499-511. doi: 10.1038/nri1391.