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本文引用的文献

1
Recognition of the immunodominant myelin basic protein peptide by autoantibodies and HLA-DR2-restricted T cell clones from multiple sclerosis patients. Identity of key contact residues in the B-cell and T-cell epitopes.来自多发性硬化症患者的自身抗体和HLA - DR2限制性T细胞克隆对免疫显性髓鞘碱性蛋白肽的识别。B细胞和T细胞表位中关键接触残基的一致性。
J Clin Invest. 1997 Sep 1;100(5):1114-22. doi: 10.1172/JCI119622.
2
Cross-reactive memory T cells for Epstein-Barr virus augment the alloresponse to common human leukocyte antigens: degenerate recognition of major histocompatibility complex-bound peptide by T cells and its role in alloreactivity.爱泼斯坦-巴尔病毒的交叉反应性记忆T细胞增强对常见人类白细胞抗原的同种异体反应:T细胞对主要组织相容性复合体结合肽的简并识别及其在同种异体反应性中的作用。
Eur J Immunol. 1997 Jul;27(7):1726-36. doi: 10.1002/eji.1830270720.
3
Triggers of autoimmune disease in a murine TCR-transgenic model for multiple sclerosis.用于多发性硬化症的小鼠TCR转基因模型中自身免疫性疾病的触发因素。
J Immunol. 1997 Jul 1;159(1):497-507.
4
Identification of high potency microbial and self ligands for a human autoreactive class II-restricted T cell clone.鉴定针对人自身反应性Ⅱ类限制性T细胞克隆的高效微生物和自身配体。
J Exp Med. 1997 May 5;185(9):1651-9. doi: 10.1084/jem.185.9.1651.
5
Molecular mimicry: can epitope mimicry induce autoimmune disease?分子模拟:表位模拟会引发自身免疫性疾病吗?
Immunol Cell Biol. 1997 Apr;75(2):113-26. doi: 10.1038/icb.1997.16.
6
Diversification of T cell responses to carboxy-terminal determinants within the 65-kD heat-shock protein is involved in regulation of autoimmune arthritis.T细胞对65-kD热休克蛋白羧基末端决定簇反应的多样化参与自身免疫性关节炎的调控。
J Exp Med. 1997 Apr 7;185(7):1307-16. doi: 10.1084/jem.185.7.1307.
7
Modifications of peptide ligands enhancing T cell responsiveness imply large numbers of stimulatory ligands for autoreactive T cells.增强T细胞反应性的肽配体修饰意味着自身反应性T细胞存在大量刺激性配体。
J Immunol. 1997 Apr 15;158(8):3746-52.
8
Differential contact of disparate class I/peptide complexes as the basis for epitope cross-recognition by a single T cell receptor.不同的I类/肽复合物的差异接触作为单个T细胞受体进行表位交叉识别的基础。
J Immunol. 1997 Apr 15;158(8):3651-8.
9
A single T cell receptor recognizes structurally distinct MHC/peptide complexes with high specificity.单个T细胞受体以高特异性识别结构不同的MHC/肽复合物。
J Exp Med. 1996 Sep 1;184(3):1017-26. doi: 10.1084/jem.184.3.1017.
10
Interferon-gamma is essential for destruction of beta cells and development of insulin-dependent diabetes mellitus.γ干扰素对于β细胞的破坏以及胰岛素依赖型糖尿病的发展至关重要。
J Exp Med. 1997 Feb 3;185(3):531-9. doi: 10.1084/jem.185.3.531.

人类病原体来源的肽激活自身反应性T细胞。

Activation of autoreactive T cells by peptides from human pathogens.

作者信息

Hausmann S, Wucherpfennig K W

机构信息

Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, MA 02115, USA.

出版信息

Curr Opin Immunol. 1997 Dec;9(6):831-8. doi: 10.1016/s0952-7915(97)80186-0.

DOI:10.1016/s0952-7915(97)80186-0
PMID:9492986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7134830/
Abstract

Activation of autoreactive T cells is a necessary-but not sufficient-step in the development of T cell mediated autoimmunity. Autoreactive T cells can be activated by viral and bacterial peptides that meet the structural requirements for MHC molecule binding and T cell receptor recognition. Due to the degenerate nature of MHC class II molecule binding motifs and a certain degree of flexibility in T cell receptor recognition, such microbial peptides have been found to be quite distinct in their primary sequence from the self-peptide they mimic.

摘要

自身反应性T细胞的激活是T细胞介导的自身免疫发展过程中的一个必要但非充分步骤。自身反应性T细胞可被符合MHC分子结合和T细胞受体识别结构要求的病毒和细菌肽激活。由于MHC II类分子结合基序的简并性以及T细胞受体识别的一定程度的灵活性,已发现此类微生物肽在其一级序列上与它们所模拟的自身肽有很大不同。