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本文引用的文献

1
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.
2
Drug hypersensitivity caused by alteration of the MHC-presented self-peptide repertoire.药物过敏反应是由 MHC 呈递的自身肽库改变引起的。
Proc Natl Acad Sci U S A. 2012 Jun 19;109(25):9959-64. doi: 10.1073/pnas.1207934109. Epub 2012 May 29.
3
Abacavir induces loading of novel self-peptides into HLA-B*57: 01: an autoimmune model for HLA-associated drug hypersensitivity.阿巴卡韦诱导新型自身肽加载到 HLA-B*57:01:一个与 HLA 相关药物过敏反应的自身免疫模型。
AIDS. 2012 Jul 17;26(11):F21-9. doi: 10.1097/QAD.0b013e328355fe8f.
4
Avidity determines T-cell reactivity in abacavir hypersensitivity.亲合力决定阿巴卡韦超敏反应中 T 细胞的反应性。
Eur J Immunol. 2012 Jul;42(7):1706-16. doi: 10.1002/eji.201142159. Epub 2012 Jun 14.
5
Drug hypersensitivity and human leukocyte antigens of the major histocompatibility complex.药物过敏反应与人类主要组织相容性复合体的白细胞抗原。
Annu Rev Pharmacol Toxicol. 2012;52:401-31. doi: 10.1146/annurev-pharmtox-010611-134701. Epub 2011 Oct 17.
6
Drug hypersensitivity: pharmacogenetics and clinical syndromes.药物过敏反应:药物遗传学与临床综合征。
J Allergy Clin Immunol. 2011 Mar;127(3 Suppl):S60-6. doi: 10.1016/j.jaci.2010.11.046.
7
Human leukocyte antigen class I-restricted activation of CD8+ T cells provides the immunogenetic basis of a systemic drug hypersensitivity.人类白细胞抗原I类分子限制的CD8 + T细胞活化提供了全身性药物超敏反应的免疫遗传学基础。
Immunity. 2008 Jun;28(6):822-32. doi: 10.1016/j.immuni.2008.04.020.
8
Activation of T cells by carbamazepine and carbamazepine metabolites.卡马西平及其代谢产物对T细胞的激活作用。
J Allergy Clin Immunol. 2006 Jul;118(1):233-41. doi: 10.1016/j.jaci.2006.03.005. Epub 2006 Apr 27.
9
Have we cut ourselves too short in mapping CTL epitopes?在绘制细胞毒性T淋巴细胞(CTL)表位图谱时,我们是否做得过于简略了?
Trends Immunol. 2006 Jan;27(1):11-6. doi: 10.1016/j.it.2005.11.001. Epub 2005 Nov 16.
10
HLA-B63 presents HLA-B57/B58-restricted cytotoxic T-lymphocyte epitopes and is associated with low human immunodeficiency virus load.HLA - B63呈现HLA - B57/B58限制性细胞毒性T淋巴细胞表位,并与低人类免疫缺陷病毒载量相关。
J Virol. 2005 Aug;79(16):10218-25. doi: 10.1128/JVI.79.16.10218-10225.2005.

涉及阿巴卡韦介导的超敏综合征的机制。

Mechanisms involved in the Abacavir-mediated hypersensitivity syndrome.

机构信息

Irsicaixa AIDS Research Institute - HIVACAT, Hospital Universitari Germans Trias i Pujol, Badalona, Spain.

出版信息

Cell Res. 2012 Dec;22(12):1637-9. doi: 10.1038/cr.2012.105. Epub 2012 Jul 10.

DOI:10.1038/cr.2012.105
PMID:22777424
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3515749/
Abstract

The potentially life-threatening adverse reactions to Abavacir (ABC), a nucleoside analog reverse transcriptase inhibitor for the treatment of HIV infection, have been known for several years to be limited to individuals expressing the HLA-B57:01 gene. Why the ABC hypersensitivity syndrome is only seen in HLA-B57:01-expressing subjects and what the precise mechanisms underlying this intolerance are remain however controversial. A series of recent studies, particularly a study by Illing et al. recently published in Nature, now answer some of these questions and offer new opportunities to better understand autoimmune disorders and prevent adverse reactions to other drugs.

摘要

阿巴卡韦(ABC)是一种用于治疗 HIV 感染的核苷类似物逆转录酶抑制剂,其可能危及生命的不良反应多年来一直仅限于表达 HLA-B57:01 基因的个体。然而,为什么 ABC 超敏反应综合征仅见于 HLA-B57:01 表达的受试者,以及这种不耐受的确切机制是什么,仍然存在争议。最近的一系列研究,特别是 Illing 等人最近在《自然》杂志上发表的研究,现在回答了其中的一些问题,并为更好地理解自身免疫性疾病和预防其他药物的不良反应提供了新的机会。