T 细胞对铍的识别。
T cell recognition of beryllium.
机构信息
Integrated Department of Immunology, National Jewish Health, Denver, CO 80206, USA.
出版信息
Curr Opin Immunol. 2013 Dec;25(6):775-80. doi: 10.1016/j.coi.2013.07.012. Epub 2013 Aug 23.
Abstract
Chronic beryllium disease (CBD) is a granulomatous lung disorder caused by a hypersensitivity to beryllium and characterized by the accumulation of beryllium-specific CD4(+) T cells in the lung. Genetic susceptibility to beryllium-induced disease is strongly associated with HLA-DP alleles possessing a glutamic acid at the 69th position of the β-chain (βGlu69). The structure of HLA-DP2, the most prevalent βGlu69-containing molecule, revealed a unique solvent-exposed acidic pocket that includes βGlu69 and represents the putative beryllium-binding site. The delineation of mimotopes and endogenous self-peptides that complete the αβTCR ligand for beryllium-specific CD4(+) T cells suggests a unique role of these peptides in metal ion coordination and the generation of altered self-peptides, blurring the distinction between hypersensitivity and autoimmunity.
摘要
慢性铍病（CBD）是一种由铍过敏引起的肉芽肿性肺部疾病，其特征是铍特异性 CD4(+)T 细胞在肺部积聚。对铍诱导疾病的遗传易感性与 HLA-DP 等位基因强烈相关，该基因具有β链第 69 位的谷氨酸（βGlu69）。HLA-DP2 的结构揭示了一个独特的溶剂暴露酸性口袋，其中包括βGlu69，代表潜在的铍结合位点。模拟表位和内源性自身肽的描绘完成了铍特异性 CD4(+)T 细胞的 αβTCR 配体，这表明这些肽在金属离子配位和产生改变的自身肽方面具有独特的作用，从而模糊了超敏反应和自身免疫之间的区别。
相似文献
1
T cell recognition of beryllium.T 细胞对铍的识别。
Curr Opin Immunol. 2013 Dec;25(6):775-80. doi: 10.1016/j.coi.2013.07.012. Epub 2013 Aug 23.
2
Linking genetic susceptibility and T cell activation in beryllium-induced disease.将遗传易感性与铍诱导疾病中的 T 细胞激活联系起来。
Proc Am Thorac Soc. 2010 May;7(2):126-9. doi: 10.1513/pats.201002-022RM.
3
Identification of beryllium-dependent peptides recognized by CD4+ T cells in chronic beryllium disease.鉴定慢性铍病中 CD4+T 细胞识别的铍依赖性肽。
J Exp Med. 2013 Jul 1;210(7):1403-18. doi: 10.1084/jem.20122426.
4
Metal-specific CD4+ T-cell responses induced by beryllium exposure in HLA-DP2 transgenic mice.铍暴露在 HLA-DP2 转基因小鼠中诱导的金属特异性 CD4 + T 细胞反应。
Mucosal Immunol. 2016 Jan;9(1):218-28. doi: 10.1038/mi.2015.54. Epub 2015 Jul 1.
5
Genetic susceptibility and immune-mediated destruction in beryllium-induced disease.铍诱导疾病中的遗传易感性和免疫介导的破坏。
Trends Immunol. 2005 Oct;26(10):543-9. doi: 10.1016/j.it.2005.08.004.
6
Beryllium presentation to CD4+ T cells is dependent on a single amino acid residue of the MHC class II beta-chain.铍向CD4+ T细胞的呈递取决于MHC II类β链的单个氨基酸残基。
J Immunol. 2005 Nov 15;175(10):7029-37. doi: 10.4049/jimmunol.175.10.7029.
7
T cell recognition in chronic beryllium disease.慢性铍病中的T细胞识别
Clin Immunol. 2006 Nov;121(2):134-43. doi: 10.1016/j.clim.2006.03.012. Epub 2006 May 12.
8
Beryllium-Induced Hypersensitivity: Genetic Susceptibility and Neoantigen Generation.铍诱导的超敏反应：遗传易感性与新抗原生成
J Immunol. 2016 Jan 1;196(1):22-7. doi: 10.4049/jimmunol.1502011.
9
Crystal structure of HLA-DP2 and implications for chronic beryllium disease.HLA-DP2 晶体结构及其对慢性铍病的影响。
Proc Natl Acad Sci U S A. 2010 Apr 20;107(16):7425-30. doi: 10.1073/pnas.1001772107. Epub 2010 Mar 31.
10
Regulatory T cells modulate granulomatous inflammation in an HLA-DP2 transgenic murine model of beryllium-induced disease.调节性 T 细胞调节 HLA-DP2 转基因小鼠铍诱导疾病模型中的肉芽肿性炎症。
Proc Natl Acad Sci U S A. 2014 Jun 10;111(23):8553-8. doi: 10.1073/pnas.1408048111. Epub 2014 May 27.
引用本文的文献
1
Interleukin-1 signaling and CD4 T cells control B cell recruitment to the lungs in chronic beryllium disease.白细胞介素-1信号传导和CD4 T细胞控制慢性铍病中B细胞向肺部的募集。
Front Immunol. 2025 Jan 28;16:1479348. doi: 10.3389/fimmu.2025.1479348. eCollection 2025.
2
Multisystemic Beryllium Disease: An Exceptional Case Revealed by a Urinary Tract Granulomatosis.多发性系统性铍病：一例泌尿道肉芽肿病揭示的特殊病例。
Int J Mol Sci. 2024 Jul 26;25(15):8166. doi: 10.3390/ijms25158166.
3
Involvement of Dendritic Cells and Th17 Cells in Induced Tertiary Lymphoid Structures in a Chronic Beryllium Disease Mouse Model.树突状细胞和 Th17 细胞在慢性铍病小鼠模型中诱导的三级淋巴样结构中的作用。
Mediators Inflamm. 2021 May 6;2021:8845966. doi: 10.1155/2021/8845966. eCollection 2021.
4
The Many Faces of CD4 T Cells: Immunological and Structural Characteristics.CD4 T细胞的多样面貌：免疫学和结构特征
Int J Mol Sci. 2020 Dec 23;22(1):73. doi: 10.3390/ijms22010073.
5
Characterization of the Class I MHC Peptidome Resulting From DNCB Exposure of HaCaT Cells.DNCB 暴露于 HaCaT 细胞后导致的 I 类 MHC 肽组学特征分析。
Toxicol Sci. 2021 Feb 26;180(1):136-147. doi: 10.1093/toxsci/kfaa184.
6
Metals and molecular carcinogenesis.金属与分子致癌作用。
Carcinogenesis. 2020 Sep 24;41(9):1161-1172. doi: 10.1093/carcin/bgaa076.
7
Metals and Mechanisms of Carcinogenesis.金属与致癌机制
Annu Rev Pharmacol Toxicol. 2019 Jan 6;59:537-554. doi: 10.1146/annurev-pharmtox-010818-021031.
8
Research to Practice Implications of High-Risk Genotypes for Beryllium Sensitization and Disease.铍致敏和疾病高风险基因型的研究对实践的启示
J Occup Environ Med. 2016 Sep;58(9):855-60. doi: 10.1097/JOM.0000000000000805.
9
Genome-wide association study of neocortical Lewy-related pathology.全基因组关联研究新皮层路易体相关病理学。
Ann Clin Transl Neurol. 2015 Sep;2(9):920-31. doi: 10.1002/acn3.231. Epub 2015 Aug 18.
10
The elements of life and medicines.生命与药物的元素。
Philos Trans A Math Phys Eng Sci. 2015 Mar 13;373(2037). doi: 10.1098/rsta.2014.0182.
本文引用的文献
1
Identification of beryllium-dependent peptides recognized by CD4+ T cells in chronic beryllium disease.鉴定慢性铍病中 CD4+T 细胞识别的铍依赖性肽。
J Exp Med. 2013 Jul 1;210(7):1403-18. doi: 10.1084/jem.20122426.
2
Immune plexins and semaphorins: old proteins, new immune functions.免疫轴蛋白和神经递质：古老的蛋白，新的免疫功能。
Protein Cell. 2013 Jan;4(1):17-26. doi: 10.1007/s13238-012-2108-4. Epub 2013 Jan 11.
3
T-cell receptor (TCR) interaction with peptides that mimic nickel offers insight into nickel contact allergy.T 细胞受体（TCR）与模拟镍的肽相互作用为了解镍接触过敏提供了线索。
Proc Natl Acad Sci U S A. 2012 Nov 6;109(45):18517-22. doi: 10.1073/pnas.1215928109. Epub 2012 Oct 22.
4
Chronic beryllium disease, HLA-DPB1, and the DP peptide binding groove.慢性铍病、HLA-DPB1 和 DP 肽结合槽。
J Immunol. 2012 Oct 15;189(8):4014-23. doi: 10.4049/jimmunol.1200798. Epub 2012 Sep 12.
5
Do MHCII-presented neoantigens drive type 1 diabetes and other autoimmune diseases?MHCII 呈递的新抗原是否会引发 1 型糖尿病和其他自身免疫性疾病？
Cold Spring Harb Perspect Med. 2012 Sep 1;2(9):a007765. doi: 10.1101/cshperspect.a007765.
6
Immune self-reactivity triggered by drug-modified HLA-peptide repertoire.药物修饰的 HLA-肽库引发的免疫自身反应性。
Nature. 2012 Jun 28;486(7404):554-8. doi: 10.1038/nature11147.
7
Mutagenesis of beryllium-specific TCRs suggests an unusual binding topology for antigen recognition.铍特异性 TCR 的诱变表明抗原识别具有不寻常的结合拓扑结构。
J Immunol. 2011 Oct 1;187(7):3694-703. doi: 10.4049/jimmunol.1101872. Epub 2011 Aug 26.
8
A highly tilted binding mode by a self-reactive T cell receptor results in altered engagement of peptide and MHC.一个自身反应性 T 细胞受体的高度倾斜结合模式导致肽和 MHC 的结合方式发生改变。
J Exp Med. 2011 Jan 17;208(1):91-102. doi: 10.1084/jem.20100725. Epub 2011 Jan 3.
9
HLA class II DPB1 and DRB1 polymorphisms associated with genetic susceptibility to beryllium toxicity.HLA Ⅱ类 DPBI 和 DRB1 多态性与铍毒性的遗传易感性相关。
Occup Environ Med. 2011 Jul;68(7):487-93. doi: 10.1136/oem.2010.055046. Epub 2010 Dec 23.
10
Crystal structure of HLA-DP2 and implications for chronic beryllium disease.HLA-DP2 晶体结构及其对慢性铍病的影响。
Proc Natl Acad Sci U S A. 2010 Apr 20;107(16):7425-30. doi: 10.1073/pnas.1001772107. Epub 2010 Mar 31.
Zotero 插件