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.
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.
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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.
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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.
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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。
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