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药物超敏反应机制阐释的最新进展。

Recent progress of elucidating the mechanisms of drug hypersensitivity.

作者信息

Hashizume Hideo

机构信息

Department of Dermatology, Shimada Municipal Hospital, Shimada, Shizuoka 427-8502, Japan.

出版信息

Asia Pac Allergy. 2012 Jul;2(3):203-9. doi: 10.5415/apallergy.2012.2.3.203. Epub 2012 Jul 25.

DOI:10.5415/apallergy.2012.2.3.203
PMID:22872823
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3406300/
Abstract

Recent technical approaches to investigating drug hypersensitivity have provided a great deal of information to solve the mechanisms that remain poorly understood. First, immunological investigations and in silico analysis have revealed that a novel interaction between T cells and antigen-presenting cells, namely the pharmacological interaction concept, is involved in drug recognition and the hapten theory. Second, progress in immunology has provided a new concept of CD4+ T cell subsets. Th17 cells have proven to be a critical player in acute generalized exanthematous pustulosis. Our recent findings suggest that this subset might contribute to the pathogenesis of Stevens-Johnson syndrome/toxic epidermal necrolysis. Third, alarmins, molecules associated with innate immunity, are also associated with exaggeration and the persistence of severe drug hypersensitivity. The latest innovative techniques are providing a new landscape to examine drug hypersensitivity.

摘要

最近用于研究药物超敏反应的技术方法为解决仍知之甚少的机制提供了大量信息。首先,免疫学研究和计算机分析表明,T细胞与抗原呈递细胞之间的一种新型相互作用,即药理学相互作用概念,参与了药物识别和半抗原理论。其次,免疫学的进展提供了CD4+ T细胞亚群的新概念。已证明Th17细胞在急性泛发性脓疱病中起关键作用。我们最近的研究结果表明,这一亚群可能与史蒂文斯-约翰逊综合征/中毒性表皮坏死松解症的发病机制有关。第三,警报素,即与固有免疫相关的分子,也与严重药物超敏反应的加剧和持续存在有关。最新的创新技术为研究药物超敏反应提供了新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/f85318049837/apa-2-203-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/81ab657e5ba1/apa-2-203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/afd7c364fc35/apa-2-203-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/1ec9dbee561f/apa-2-203-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/21c399d635a2/apa-2-203-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/f85318049837/apa-2-203-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/81ab657e5ba1/apa-2-203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/afd7c364fc35/apa-2-203-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/1ec9dbee561f/apa-2-203-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/21c399d635a2/apa-2-203-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c377/3406300/f85318049837/apa-2-203-g005.jpg

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本文引用的文献

1
15 kDa granulysin causes differentiation of monocytes to dendritic cells but lacks cytotoxic activity.15 kDa 颗粒溶素可诱导单核细胞分化为树突状细胞,但无细胞毒性。
J Immunol. 2012 Jun 15;188(12):6119-26. doi: 10.4049/jimmunol.1200570. Epub 2012 May 14.
2
Direct interaction between HLA-B and carbamazepine activates T cells in patients with Stevens-Johnson syndrome.直接的 HLA-B 与卡马西平相互作用会激活史蒂文斯-约翰逊综合征患者的 T 细胞。
J Allergy Clin Immunol. 2012 Jun;129(6):1562-9.e5. doi: 10.1016/j.jaci.2011.12.990. Epub 2012 Feb 8.
3
High-mobility group box 1 protein (HMGB1) as a novel diagnostic tool for toxic epidermal necrolysis and Stevens-Johnson syndrome.
高迁移率族蛋白B1(HMGB1)作为中毒性表皮坏死松解症和史蒂文斯-约翰逊综合征的一种新型诊断工具。
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Impairment of regulatory capacity of CD4+CD25+ regulatory T cells mediated by dendritic cell polarization and hyperthyroidism in Graves' disease. Graves 病中树突状细胞极化和甲状腺功能亢进导致 CD4+CD25+调节性 T 细胞调节功能障碍。
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Genome-wide association study identifies HLA-A*3101 allele as a genetic risk factor for carbamazepine-induced cutaneous adverse drug reactions in Japanese population.全基因组关联研究发现 HLA-A*3101 等位基因是日本人群卡马西平诱导皮肤不良反应的遗传风险因素。
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DAMPening inflammation by modulating TLR signalling.通过调节 TLR 信号抑制炎症。
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Granulysin activates antigen-presenting cells through TLR4 and acts as an immune alarmin.颗粒酶 B 通过 TLR4 激活抗原呈递细胞,并充当免疫警报素。
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CD94/NKG2C is a killer effector molecule in patients with Stevens-Johnson syndrome and toxic epidermal necrolysis.CD94/NKG2C 是 Stevens-Johnson 综合征和中毒性表皮坏死松解症患者中的一种杀伤效应分子。
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