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Code  ›  人类白细胞抗原基因的遗传变异与药物不良反应的关系 - PMC
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10930308/
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Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2021 Apr 28; 46(4): 404–413.
Chinese. doi: 10.11817/j.issn.1672-7347.2021.200256
PMCID: PMC10930308
PMID: 33967088

Language: Chinese | English

人类白细胞抗原基因的遗传变异与药物不良反应的关系

Progress in study on the association between HLA genetic variation and adverse drug reactions

刘 雅婷 , 1, 2 曾 祥昌 , 1, 2 and 欧阳 冬生 corresponding author 1, 2, 3

刘 雅婷

中南大学湘雅医院临床药理研究所, 410008

中南大学临床药理研究所， 遗传药理学湖南省重点实验室, 410078

Find articles by 刘 雅婷

曾 祥昌

中南大学湘雅医院临床药理研究所, 410008

中南大学临床药理研究所， 遗传药理学湖南省重点实验室, 410078

Find articles by 曾 祥昌

欧阳 冬生

中南大学湘雅医院临床药理研究所, 410008

中南大学临床药理研究所， 遗传药理学湖南省重点实验室, 410078

复杂基质样本生物分析湖南省重点实验室, 中南大学湘雅医院临床药理研究所, 410008

中南大学临床药理研究所， 遗传药理学湖南省重点实验室, 410078
复杂基质样本生物分析湖南省重点实验室, 410205
corresponding author Corresponding author.
欧阳冬生 ，Email: nc.ude.usc@049108 , ORCID: 0000-0002-1743-8610
HLA 结构与功能

HLA是一组高度保守且与抗原识别有关的细胞表面蛋白，是目前已知的人类最复杂的基因，位于6号染色体短臂上。HLA等位基因通常分为I、II、III基因编码区。位于I和II基因编码区的基因可进一步分为经典HLA基因与非经典HLA基因，经典HLA基因与抗原递呈有关；III基因编码区的基因主要编码分泌蛋白，与炎症相关。

将抗原递呈给T淋巴细胞是HLA最主要的功能。经典HLA-I类基因(HLA-A、HLA-B、HLA-C)编码的HLA蛋白分子递呈内源性抗原肽，可被CD8 + T细胞识别；经典的HLA-II类基因(HLA-DPA1、HLA-DPB1、HLA-DQA1、HLADQB1、HLA-DRA、HLA-DRB1)编码的HLA蛋白分子向CD4 + T细胞递呈外源性抗原肽，参与免疫应答和免疫调节 [ 4 ] 。

HLA基因的多态性可引起HLA抗原结合槽形状和电化学结构变化 [ 5 - 6 ] 。不同HLA抗原结合槽的特异性决定了HLA分子递呈抗原的选择性，也是免疫应答个体差异的基础。大量研究 [ 7 - 9 ] 显示HLA遗传变异是IADRs重要的易感因素。肝和皮肤作为重要的代谢器官，免疫功能活跃，是HLA相关ADRs最常累及的器官 [ 5 ] 。

2. HLA 多态性与严重皮肤不良反应

严重皮肤不良反应(severe cutaneous adverse reac-tions，SCARs)是一组与剂量无关的潜在致命ADRs。SCARs属于B类ADRs中的IV型超敏反应，即T细胞介导的迟发型药物过敏反应，包括史蒂文斯-约翰逊综合征(Stevens-Johnson syndrome，SJS)、中毒性表皮坏死溶解症(toxic epidermal necrolysis，TEN)、急性全身性皮疹性脓疱病(acute generalized exanthe-matous pustulosis，AGEP)、嗜酸性粒细胞增多与全身症状复杂的药物反应(drug reaction with eosinophilia and systemic symptoms complex，DRESS)和药物超敏反应综合征(drug-induced hypersensitivity syndrome，DIHS) [ 10 - 11 ] 。HLA等位基因与多种药物诱导的SCARs相关( 表1 )，其中HLA-B*15:02基因与卡马西平/磷苯妥英/奥卡西平、HLA-A*31:01基因与卡马西平、HLA-B*57:01基因与阿巴卡韦等被写入美国食品药品管理局(Food and Drug Administration，FDA)药品标签警告。

表1

HLA 等位基因与 SCARs

Table 1 HLA allelic genes and SCARs

基因型 药物 ADR 人群 OR 参考文献
HLA-A*02:01 丹参酮 MPE/SJS/TEN 中国人 5.1*，7.1† [ 48 ]
HLA-A*02:07 唑尼沙胺 SJS/TEN 日本人 9.8† [ 49 ]
HLA-A*31:01 卡马西平 SJS 欧洲人 25.9† [ 22 ]
HLA-A*32:01 万古霉素 DRESS 欧洲人 — [ 50 ]
HLA-B*13:01 氨苯砜 DRESS 中国人 20.5† [ 51 ]
苯妥英 SJS/TEN 中国人 3.7* [ 13 ]
HLA-B*15:02 卡马西平 SJS 东南亚人 2504.0*，895.0† [ 14 ]
苯妥英 SJS/TEN 马来人 5.7*，8.6† [ 52 ]
拉莫三嗪 SJS/TEN 中国人 5.1* [ 13 ]
复方新诺明 SJS/TEN 泰国人 3.9*，2.4† [ 53 ]
奥卡西平 SJS 中国人 27.9* [ 54 ]
奥卡西平 SJS 泰国人 49.0* [ 54 ]
HLA-B*15:13 苯妥英 SJS/TEN 马来人 11.3*，8.6† [ 52 ]
HLA-B*15:21 卡马西平 SJS/TEN 菲律宾人 7.5* [ 55 ]
HLA-B*40:02 奥卡西平 MPE 韩国人 4.3*，4.0† [ 56 ]
HLA-B*51:01 苯巴比妥 SJS/TEN 日本人 16.7† [ 49 ]
HLA-B*57:01 阿巴卡韦 DIHS 澳大利亚人 117.0* [ 27 ]
基因型 药物 ADR 人群 OR 参考文献
HLA-B*58:01 别嘌呤醇 SJS/TEN 中国人 580.3*，393.5† [ 38 ]
HLA-B*59:01 醋甲唑胺 SJS/TEN 中国人 305.0*，1 974.0† [ 57 ]
HLA-C*04:01 奈韦拉平 SJS 马拉维人 17.5* [ 58 ]
HLA-B*35-Cw*04 奈韦拉平 SJS 亚洲人 18.3† [ 59 ]
HLA-C*06:02 复方新诺明 SJS/TEN 泰国人 11.8*，1.9† [ 53 ]
HLA-C*08:01 复方新诺明 SJS/TEN 泰国人 3.5*，2.1† [ 53 ]
HLA-DQA1*02:01-DRB1*07:01-DQB1*02:02 天冬酰胺酶 DIHS 匈牙利人 5.0* [ 60 ]
HLA-DRB1*04:03 奥卡西平 MPE 韩国人 14.6*，3.1† [ 56 ]
HLA-DRB1*16:02 苯妥英 SJS/TEN 中国人 4.3* [ 13 ]

*与药物耐受组比较；†与健康人群比较。MPE：斑丘疹；SJS：史蒂文斯-约翰逊综合征；TEN：中毒性表皮坏死溶解症；DRESS：全身症状复杂的药物反应；DIHS：药物超敏反应综合征。

2.1. HLA-B*15:02 基因

HLA-B*15:02基因是芳香类抗癫痫药(如卡马西平、苯妥英钠、奥卡西平、拉莫三嗪)SCARs的潜在危险因素 [ 12 - 13 ] 。2004年有研究 [ 14 ] 首次报道中国台湾人HLA-B*15:02等位基因与卡马西平诱导的SJS强相关，随后被在中国香港、印度、马来西亚、泰国人群中展开的病例对照研究 [ 15 - 18 ] 所证实。多国提出警示并建议亚洲患者在接受卡马西平治疗之前进行HLA-B*15:02基因检测，并已取得了积极效果 [ 19 - 20 ] 。

HLA-B*15:02基因与卡马西平诱导SCARs的相关性具有种族差异，推测其可能与HLA-B*15:02基因表达的种族差异有关 [ 21 - 22 ] 。但HLA-B*15:02基因不是卡马西平诱导SCARs必备和唯一的易感等位基因 [ 21 , 23 ] ，如HLA-A*31:01基因是日本和欧洲人群卡马西平诱导SCARs的易感等位基因 [ 22 , 24 ] 。

卡马西平诱导SCARs的分子机制尚未完全阐明，有研究 [ 25 ] 表明不同基因遵循不同的分子机制。

2.2. HLA-B*57:01 基因

HLA-B*57:01基因与多种ADRs相关，如阿巴卡韦诱发的DIHS [ 26 - 27 ] 、氟氯西林和帕唑帕尼诱导的药物性肝损伤(drug-induced liver injury，DILI) [ 28 - 29 ] 。多中心、大样本前瞻性研究 [ 30 ] 结果显示：HLA-B*57:01基因筛查组阿巴卡韦诱导的DIHS发病率(3.4%)明显低于非筛查对照组(7.8%)，表明基因检测具有预防特定ADRs的价值。欧洲药品管理局(European Medicines Agency，EMA)和美国FDA建议对接受阿巴卡韦治疗的患者进行HLA-B*57:01基因筛查 [ 31 - 32 ] 。

目前认为，阿巴卡韦诱导DIHS的发生机制可能是通过“改变肽库”、激活T细胞，从而诱发DIHS [ 33 - 34 ] 。此外，在HLA-B*57:01转基因鼠中发现下调CD4 + T细胞、干预免疫检查点、创造炎症微环境能增加阿巴卡韦诱导的ADRs发生率 [ 35 - 37 ] ，但缺乏临床研究支持。

2.3. HLA-B*58:01 基因

HLA-B*58:01基因为别嘌呤醇诱发SCARs的高风险基因 [ 38 - 40 ] 。在肾功能不全患者中，HLA-B*58:01基因对预测别嘌呤醇诱导的SCARs具有更高的准确性 [ 41 ] 。也有研究 [ 20 ] 显示：给予HLA-B*58:01基因阳性携带者替代药物治疗，能显著降低SCARs发生率。中国台湾食品药品监督管理局、美国风湿病学会、韩国国民健康保险先后建议对需要别嘌呤醇治疗的患者进行HLA-B*58:01基因检测 [ 42 - 43 ] 。

目前认为，其发生机制可能与HLA-B*58:01基因Arg97残基结合别嘌呤醇或其代谢物氧嘌呤醇后的继发药理作用有关 [ 44 ] 。

2.4. HLA-A*02:01 基因

HLA-A*02:01基因是拉莫三嗪诱导墨西哥患者斑丘疹(maculopapular exanthema，MPE)以及阿莫西林-克拉维酸钾诱导欧洲西北部人群DILI的风险基因 [ 45 - 46 ] 。随着HLA基因多态性与中药诱导SCARs相关的研究 [ 47 - 48 ] 相继展开，HLA-A*02:01基因也可作为丹参酮汉族人个体化治疗的潜在预测指标 [ 48 ] 。另外，分子对接实验 [ 48 ] 证实：丹参酮多个成分与HLA-A*02:01基因有较高亲和力(≤-7.5 kcal/mol)。

3. HLA 与 IDILI

HLA基因多态性与特异质药物性肝损伤(idiosyncratic drug-induced liver injury，IDILI)关系密切( 表2 )，部分药物所致IDILI与多个HLA位点相关。HLA与IDILI相关的事实提示了适应性免疫在IDILI过程中的重要作用，但具体机制有待进一步明确。

表2

HLA 等位基因与 IDILI

Table 2 HLA allelic genes and IDILI

基因型 药物 人群 OR 参考文献
HLA-A*02:01-DQB1*06:02 阿莫西林-克拉维酸钾 欧洲西北部人，西班牙人 2.2† [ 46 ]
HLA-A*33:01 特比奈芬 欧洲人 40.5† [ 69 ]
甲基多巴 欧洲人 97.8†
非诺贝特 欧洲人 58.7†
噻氯匹定 欧洲人 163.1†
HLA-A*33:03 噻氯匹定 日本人 13.0* [ 74 ]
HLA-B*14:01 复方新诺明 美籍欧洲人 9.2† [ 75 ]
HLA-B*35:01 何首乌 中国人 86.5‡，143.9† [ 76 ]
复方新诺明 美籍非洲人 — [ 75 ]
HLA-B*35:02 米诺环素 欧洲人 29.6† [ 77 ]
HLA-B*39:01 英夫利昔 欧洲人 43.6* [ 78 ]
HLA-B*57:01 氟氯西林 欧洲人 80.6* [ 28 ]
帕唑帕尼 多种族 — [ 29 ]
HLA-B*57:03 氟氯西林 欧洲人 79.2† [ 65 ]
HLA-B*58:01 奈韦拉平 南非人 3.8* [ 79 ]
HLA-DQA1*01:02 罗美昔布 多种族 6.3* [ 62 ]
HLA-DQA1*02 希美加群 瑞典人 4.4* [ 80 ]
HLA-DQA1*02:01 拉帕替尼 多种族 14.1† [ 81 ]
HLA-DQB1*06:02 罗美昔布 多种族 6.9* [ 62 ]
HLA-DRB1*01:01 奈韦拉平 多种族 3.7* [ 82 ]
HLA-DRB1*01:02 奈韦拉平 南非 4.7* [ 79 ]
HLA-DRB1*07:01 拉帕替尼 多种族 14.1† [ 81 ]
HLA-DRB1*07 希美加群 瑞典 4.4* [ 80 ]
HLA-DRB1*15:01 罗美昔布 多种族 7.5* [ 62 ]
HLA-DRB1*15:01-DRB5*01:01-DQB1*06:02 阿莫西林-克拉维酸钾 比利时人 — [ 61 ]
HLA-DRB1*16:01-DQB1*05:02 氟吡汀 德国人 18.7† [ 83 ]
HLA-DRB5*01:01 罗美昔布 多种族 7.2* [ 62 ]

*与药物耐受组比较；†与健康人群比较；‡与其他DILI比较。

3.1. HLA-DRB1*15:01-DRB5*01:01-DQB1*06:02 单倍型

Hautekeete等 [ 61 ] 首次报道了在比利时白人中HLA-DRB1*15:01-DRB5*01:01-DQB1*06:02单倍型与阿莫西林-克拉维酸钾诱导的DILI具有显著相关性，结果显示20/30病例组(57.1%)同时携带HLA-DRB1*15:01、DRB5*01:01和DQB1*06:02基因，远高于对照组(11.7%)。这一结论被2011年在欧洲和美国白人中展开的一项全基因组关联分析 [ 46 ] 证实。此外，HLA-DRB1*15:01-DRB5*01:01-DQB1*06:02单倍型还与罗美昔布诱导的DILI有关 [ 62 ] 。

可见，HLA风险基因在化学结构不同的药物引起的ADRs中具有重叠性，但相同风险基因与不同药物引起的ADRs之间的相关性有较大差异。现有研究 [ 63 - 64 ] 认为：“半抗原机制”可能是HLA介导阿莫西林-克拉维酸钾DILI的机制，罗美昔布致DILI机制研究尚未见报道，因此，尚无解释这种重叠性以及差异性的机制理论。

3.2. HLA-B*57:01 基因

HLA-B*57:01基因是氟氯西林DILI以及帕唑帕尼DILI的风险预测因子 [ 28 - 29 ] ，但二者OR值以及阳性预测率相差较大的原因尚未阐明。最新研究 [ 65 ] 支持了先前的发现，并且提出HLA-B*57:03同样是氟氯西林DILI的易感基因(OR=79.21； P <0.01)。值得注意的是，HLA-B*57:01与HLA-B*57:03基因序列高度同源，肽库具有较大程度重叠 [ 66 ] 。

体外研究 [ 67 - 68 ] 表明：HLA-B*57:01基因可通过“半抗原机制”以及“药理作用机制”参与氟氯西林诱导的T细胞激活。目前，未见帕唑帕尼DILI分子机制研究，具有相同风险因子的阿巴卡韦诱导DIHS的机制研究或许能为氟氯西林、帕唑帕尼DILI潜在机制研究提供参考。

3.3. HLA-A*33:01 基因

不同于以往的只涉及一种特定药物的鉴定一个或多个HLA风险等位基因的病例对照研究，Nicoletti等 [ 69 ] 通过全基因组关联研究(genome-wide association study，GWAS)考察了引起DILI的药物组与HLA基因多态性的关系，发现HLA-A*33:01基因可能是多种DILI的风险基因。其中，与HLA-A*33:01基因最相关的药物是特比萘芬、非诺贝特和噻氯匹定，三者主要以代谢物的形式被排出体外，暗示HLA-A*33:01基因与胆汁淤积型以及混合型DILI有更强相关性。该研究还表明HLA-A*33:01-B*14:02-C*08:02单倍型与特比萘芬DILI相关性更强。

分子对接实验 [ 34 , 70 ] 显示：特比萘芬与HLA-A*33:01、HLA-B*14:02分子的结合位置和阿巴卡韦与HLA-B*57:01分子的结合位置相同，推测二者具有相似作用机制。

3.4. HLA-B*35:01 基因

特异性HLA基因作为生物标志物的可能性也存在于中药DILI中。Aithal [ 71 ] 发现携带HLA-B*35:01基因携带者在使用何首乌时，罹患DILI的风险更高(OR=30.4，95% CI：11.7~77.1， P <0.01)。这是首个中草药引起的DILI与HLA基因多态性关系的研究，有力地证实了个体易感性在中药DILI中的重要作用，被国际著名肝病学专家Guruprasad Aithal誉为“转化医学研究的优秀范例”。个体遗传差异与何首乌的关系也作为重要内容被写入《何首乌安全用药指南》 [ 72 ] 。

尽管有学者 [ 73 ] 构建了基于内毒素的何首乌IDILI评价模型，但该模型并未真正反映何首乌DILI的临床特征(如迟发性、再激发现象)。适应性免疫可能会更好地解释个体对何首乌诱导的免疫介导的IDILI的敏感性差异。

4. HLA 与其他 ADRs

除SCARs和DILI外，也不乏其他ADRs与HLA的相关性研究( 表3 )。如HLA-B*38:02和HLA-DRB1*08:03基因与抗甲状腺药物诱导的粒细胞缺乏症密切相关 [ 84 ] ，HLA-DRB1*08:02基因与布西拉明诱导的蛋白尿有关 [ 85 ] ，HLA-A*31:01基因与甲氨蝶呤诱导的间质性肺病有关 [ 86 ] 。

表3

HLA 等位基因与其他 ADRs

Table 3 HLA allelic genes and other ADRs

基因型 药物 ADR 人群 OR 参考文献
HLA-A*31:01 甲氨蝶呤 间质性肺病 日本人 3.0* [ 86 ]
柳氮磺吡啶 粒性白血球缺乏症 瑞典人、西班牙人、德国人 4.8* [ 87 ]
HLA-B*08:01 柳氮磺吡啶 粒性白血球缺乏症 瑞典人、西班牙人、德国人 2.3* [ 87 ]
HLA-B*27:05 抗甲状腺药 粒性白血球缺乏症 欧洲人 16.9*，7.3† [ 88 ]
HLA-B*38:02 抗甲状腺药 粒性白血球缺乏症 中国人 21.5* [ 84 ]
HLA-B*59:01 氯氮平 粒性白血球缺乏症 日本人 6.3*，10.7† [ 89 ]
HLA-DQA1*02:01-DRB1*07:01 咪唑硫嘌呤 胰腺炎 加拿大人 4.2~15.9* [ 90 ]
HLA-DRB1*08:02 布西拉明 蛋白尿 日本人 25.2* [ 85 ]
HLA-DRB1*08:03 抗甲状腺药 粒性白血球缺乏症 中国人 6.1* [ 84 ]
HLA-DRB1*11:01 他汀类 肌病 欧洲人、美籍非洲人 8.3*，11.7† [ 91 ]

*与药物耐受组比较；†与健康人群比较。

5. 介导 ADRs 的免疫机制

HLA依赖的ADRs分子机制尚未被阐明，现有4种学说，分别为半抗原学说、药理作用学说、改变肽库学说和改变T细胞受体(T cell receptor，TCR)学说。

5.1. 半抗原学说

不具有免疫原性的小分子药物与蛋白质不可逆结合后，由抗原递呈细胞(antigen presenting cell，APC)递呈给T细胞，触发免疫应答 [ 92 ] ，如阿莫西林-克拉维酸钾DILI [ 63 ] 和氟氯西林DILI [ 68 , 93 ] 。免疫介导的DILI发生率比半抗原模型所预测的低，推测肝耐受机制发挥了作用 [ 94 ] 。此外，“半抗原学说”未能解释药物引起的全身性过敏反应 [ 95 ] 。

5.2. 药理作用学说

药物或其活性代谢物不需要与抗原肽结合成新抗原，可直接与HLA/TCR非共价结合，干预细胞膜表面受体的相互识别 [ 4 , 7 ] ，如卡马西平及别嘌呤醇诱导的SCARs [ 44 , 96 ] 。该学说可以解释药物引起的全身性过敏反应，也给反应活性小的分子(如天然产物、中药)诱发ADRs提供了依据 [ 95 ] 。

5.3. 改变肽库学说

HLA基因多态性的功能差异主要体现在抗原结合槽区域，不同HLA分子递呈的抗原范围不同。小分子非共价结合到HLA抗原结合槽，从而改变肽结合的特异性 [ 97 ] 。阿巴卡韦与HLA-B*57:01蛋白的“F口袋”结合，改变了抗原结合槽的化学性质和构象，所递呈的肽库发生变化，进而引发免疫反应 [ 33 - 34 ] 。

5.4. 改变 TCR 学说

部分药物(如磺胺甲恶唑)作为抗原与特定的TCR结合并改变TCR的构象，使其具有与HLA-内源肽复合物结合以引发免疫反应的潜力 [ 11 ] 。针对TCR与HLA依赖性ADRs的免疫基础研究，可为阐明ADRs的发病机制、寻找新的治疗方法提供思路。

6. 展 望

近年来HLA与ADRs的关联研究取得了重要进展，尤其在天然药物和中药领域。这些关联被写进医学指南和药品说明书，进一步纳入临床合理用药软件中的医药信息数据库，可为防范和减少ADRs提供更便捷的依据，发挥临床预测以及辅助诊断ADRs的潜力，提高临床用药有效性和安全性，减少医护人员的工作压力，对个体化医疗具有深远意义。准确识别HLA遗传多样性引起的ADRs风险将提高已上市药品临床使用的安全性，减少医疗成本。

尽管HLA与ADRs的关联研究丰富并推动了对其免疫发病机制的了解，但同一种药物在不同的个体中会导致不同的临床表型的原因仍然未知。目前大多数研究都围绕单个免疫机制展开，将这些假说进行协同互补考虑是今后研究的方向，因为上述机制学说各有优点与局限，ADRs的发生可能同时依赖多个机制。不同体外实验推测的免疫机制不一致，难以建立与临床表型的联系，因此需要借助有效的动物模型阐明复杂机制。

此外，未来需要建立和完善国内甚至国际层面的多中心合作体系，克服局部样本量较少的困难；协同考虑HLA以外的影响因素，提高阳性预测率。有理由相信，一些经典的不可预测的特异质ADRs在未来将变得可预测、可预防，药品监管法律、法规体系将更完善，药物设计和开发将更合理，公众用药将更安全有效。

基金资助

国家“重大新药创制”科技重大专项(2017ZX09304014)；湖南省重点研发计划(2019SK2241)；湖南省创新创业投资项目(2019GK5020)；湖南创新型省份建设专项创新平台(2019CB1014)。

The work was supported by the National Development of Key Novel Drugs for Special Projects (2017ZX09304014), the Key Research and Development Programs of Hunan Province (2019SK2241), the Innovation and Entrepreneurship Investment Project in Hunan Province (2019GK5020), the International Scientific and Technological Innovation Cooperation Base for Bioanalysis of Complex Matrix Samples in Hunan Province (2019CB1014), China.

利益冲突声明

作者声称无任何利益冲突。

原文网址

http://xbyxb.csu.edu.cn/xbwk/fileup/PDF/202104404.pdf

参考文献

1. Chan SL, Ng HY, Sung C, et al.. Economic burden of adverse drug reactions and potential for pharmacogenomic testing in Singaporean adults [J]. Pharmacogenomics J , 2018, 19 ( 4 ): 401-410. [ PubMed ] [ Google Scholar ]
2. Coleman J, Pontefract S. Adverse drug reactions [J]. Clin Med (Lond) , 2016, 16 ( 5 ): 481-485. [ PMC free article ] [ PubMed ] [ Google Scholar ]
3. Schlosstein L, Terasaki PI, Bluestone R, et al.. High association of an HL-A antigen, W27, with ankylosing spondylitis [J]. N Engl J Med , 1973, 288 ( 14 ): 704-706. [ PubMed ] [ Google Scholar ]
4. Fan WL, Shiao MS, Hui RC, et al.. HLA association with drug-induced adverse reactions [J]. J Immunol Res , 2017, 2017 : 3186328. [ PMC free article ] [ PubMed ] [ Google Scholar ]
5. Usui T, Naisbitt D. Human leukocyte antigen and idiosyncratic adverse drug reactions [J]. Drug Metab Pharmacokinet , 2017, 32 ( 1 ): 21-30. [ PubMed ] [ Google Scholar ]
6. Illing P, Mifsud N, Purcell A. Allotype specific interactions of drugs and HLA molecules in hypersensitivity reactions [J]. Curr Opin Immunol , 2016, 42 : 31-40. [ PubMed ] [ Google Scholar ]
7. Pavlos R, Mallal S, Ostrov D, et al.. T cell-mediated hypersensitivity reactions to drugs [J]. Annu Rev Med , 2015, 66 ( 1 ): 439-454. [ PMC free article ] [ PubMed ] [ Google Scholar ]
8. Mosedale M, Watkins PB. Understanding idiosyncratic toxicity: Lessons learned from drug-induced liver injury [J]. J Med Chem , 2020, 63 ( 12 ): 6436-6461. [ PubMed ] [ Google Scholar ]
9. Chang C, Chen C, Hung S, et al.. Pharmacogenetic testing for prevention of severe cutaneous adverse drug reactions [J]. Front Pharmacol , 2020, 11 : 969. [ PMC free article ] [ PubMed ] [ Google Scholar ]
10. Sasidharanpillai S, Riyaz N, Khader A, et al.. Severe cutaneous adverse drug reactions: a clinicoepidemiological study [J]. Indian J Dermatol , 2015, 60 ( 1 ): 102. [ PMC free article ] [ PubMed ] [ Google Scholar ]
11. Chen CB, Abe R, Pan RY, et al.. An updated review of the molecular mechanisms in drug hypersensitivity [J]. J Immunol Res , 2018, 2018 : 6431694. [ PMC free article ] [ PubMed ] [ Google Scholar ]
12. Mullan KA, Anderson A, Illing PT, et al.. HLA-associated antiepileptic drug-induced cutaneous adverse reactions [J]. HLA , 2019, 93 ( 6 ): 417-435. [ PubMed ] [ Google Scholar ]
13. Hung S, Chung W, Liu Z, et al.. Common risk allele in aromatic antiepileptic-drug induced Stevens-Johnson syndrome and toxic epidermal necrolysis in Han Chinese [J]. Pharmaco-genomics , 2010, 11 ( 3 ): 349-356. [ PubMed ] [ Google Scholar ]
14. Chung WH, Hung SI, Hong HS, et al.. A marker for Stevens-Johnson syndrome [J]. Nature , 2004, 428 ( 6982 ): 486-486. [ PubMed ] [ Google Scholar ]
15. Man CB, Kwan P, Baum L, et al.. Association between HLA-B*1502 allele and antiepileptic drug-induced cutaneous reactions in Han Chinese [J]. Epilepsia , 2007, 48 ( 5 ): 1015-1018. [ PubMed ] [ Google Scholar ]
16. Chang CC, Too CL, Murad S, et al.. Association of HLA-B*1502 allele with carbamazepine-induced toxic epidermal necrolysis and Stevens-Johnson syndrome in the multi-ethnic Malaysian population [J]. Int J Dermatol , 2011, 50 ( 2 ): 221-224. [ PubMed ] [ Google Scholar ]
17. Locharernkul C, Loplumlert J, Limotai C, et al.. Carbamazepine and phenytoin induced Stevens-Johnson syndrome is associated with HLA-B*1502 allele in Thai population [J]. Epilepsia , 2008, 49 ( 12 ): 2087-2091. [ PubMed ] [ Google Scholar ]
18. Aggarwal R, Sharma M, Modi M, et al.. HLA-B*1502 is associated with carbamazepine induced Stevens-Johnson syndrome in North Indian population [J]. Hum Immunol , 2014, 75 ( 11 ): 1120-1122. [ PubMed ] [ Google Scholar ]
19. Tan-Koi WC, Sung C, Chong YY, et al.. Tailoring of recommendations to reduce serious cutaneous adverse drug reactions: a pharmacogenomics approach [J]. Pharmacogenomics , 2017, 18 ( 9 ): 881-890. [ PubMed ] [ Google Scholar ]
20. Ko TM, Tsai CY, Chen SY, et al.. Use of HLA-B*58: 01 genotyping to prevent allopurinol induced severe cutaneous adverse reactions in Taiwan: national prospective cohort study [J]. BMJ , 2015, 351 : h4848. [ PMC free article ] [ PubMed ] [ Google Scholar ]
21. Kaniwa N, Saito Y, Aihara M, et al.. HLA-B*1511 is a risk factor for carbamazepine-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in Japanese patients [J]. Epilepsia , 2010, 51 ( 12 ): 2461-2465. [ PubMed ] [ Google Scholar ]
22. Mccormack M, Alfirevic A, Bourgeois S, et al.. HLA-A*3101 and carbamazepine-induced hypersensitivity reactions in Europeans [J]. N Engl J Med , 2011, 364 ( 12 ): 1134-1143. [ PMC free article ] [ PubMed ] [ Google Scholar ]
23. Ikeda H, Takahashi Y, Yamazaki E, et al.. HLA class I markers in Japanese patients with carbamazepine-induced cutaneous adverse reactions [J]. Epilepsia , 2010, 51 ( 2 ): 297-300. [ PubMed ] [ Google Scholar ]
24. Mushiroda T, Takahashi Y, Onuma T, et al.. Association of HLA-A*31: 01 screening with the incidence of carbamazepine- induced cutaneous adverse reactions in a Japanese population [J]. JAMA Neurol , 2018, 75 ( 7 ): 842-849. [ PMC free article ] [ PubMed ] [ Google Scholar ]
25. Simper GS, Graser LS, Celik AA, et al.. The mechanistic differences in HLA-associated carbamazepine hypersensitivity [J]. Pharmaceutics , 2019, 11 ( 10 ): 536. [ PMC free article ] [ PubMed ] [ Google Scholar ]
26. Hetherington S, Hughes AR, Mosteller M, et al.. Genetic variations in HLA-B region and hypersensitivity reactions to abacavir [J]. Lancet , 2002, 359 ( 9312 ): 1121-1122. [ PubMed ] [ Google Scholar ]
27. Mallal S, Nolan D, Witt C, et al.. Association between presence of HLA-B*5701, HLA-DR7, and HLA-DQ3 and hypersensitivity to HIV-1 reverse-transcriptase inhibitor abacavir [J]. Lancet , 2002, 359 ( 9308 ): 727-732. [ PubMed ] [ Google Scholar ]
28. Daly AK, Donaldson PT, Bhatnagar P, et al.. HLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin [J]. Nat Genet , 2009, 41 ( 7 ): 816-819. [ PubMed ] [ Google Scholar ]
29. Xu CF, Johnson T, Wang X, et al.. HLA-B*57: 01 confers susceptibility to Pazopanib-associated liver injury in patients with cancer [J]. Clin Cancer Res , 2016, 22 ( 6 ): 1371-1377. [ PMC free article ] [ PubMed ] [ Google Scholar ]
30. Mallal S, Phillips E, Carosi G, et al.. HLA-B*5701 screening for hypersensitivity to abacavir [J]. N Engl J Med , 2008, 358 ( 6 ): 568-579. [ PubMed ] [ Google Scholar ]
31. European Medicines Agency . Ziagen: iEPAR-product information (PDF/3.84 MB) (updated) [EB/OL]. (2021-02-24)[2021-02-24]. https://www.ema.europa.eu/en/medicines/human/EPAR/ziagen .
32. U.S. Food and Drug Administration . Table of pharmacogenomic biomarkers in drug labeling [EB/OL]. (2020-08-18)[2021-02-24]. https://www.fda.gov/drugs/science-and-research-drugs/table-pharmacogenomic-biomarkers-drug-labeling .
33. Illing PT, Vivian JP, Dudek NL, et al.. Immune self-reactivity triggered by drug-modified HLA-peptide repertoire [J]. Nature , 2012, 486 ( 7404 ): 554-558. [ PubMed ] [ Google Scholar ]
34. Ostrov DA, Grant BJ, Pompeu YA, et al.. Drug hypersensitivity caused by alteration of the MHC-presented self-peptide repertoire [J]. Proc Natl Acad Sci USA , 2012, 109 ( 25 ): 9959-9964. [ PMC free article ] [ PubMed ] [ Google Scholar ]
35. Cardone M, Garcia K, Tilahun ME, et al.. A transgenic mouse model for HLA-B*57: 01-linked abacavir drug tolerance and reactivity [J]. J Clin Invest , 2018, 128 ( 7 ): 2819-2832. [ PMC free article ] [ PubMed ] [ Google Scholar ]
36. Susukida T, Aoki S, Kogo K, et al.. Evaluation of immune-mediated idiosyncratic drug toxicity using chimeric HLA transgenic mice [J]. Arch Toxicol , 2018, 92 ( 3 ): 1177-1188. [ PubMed ] [ Google Scholar ]
37. Song B, Aoki S, Liu C, et al.. An animal model of abacavir-induced HLA-mediated liver injury [J]. Toxicol Sci , 2018, 162 ( 2 ): 713-723. [ PubMed ] [ Google Scholar ]
38. Hung S, Chung W, Liou L, et al.. HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol [J]. Proc Natl Acad Sci USA , 2005, 102 ( 11 ): 4134-4139. [ PMC free article ] [ PubMed ] [ Google Scholar ]
39. Tassaneeyakul W, Jantararoungtong T, Chen P, et al.. Strong association between HLA-B*5801 and allopurinol-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in a Thai population [J]. Pharmacogenet Genomics , 2009, 19 ( 9 ): 704-709. [ PubMed ] [ Google Scholar ]
40. Lonjou C, Borot N, Sekula P, et al.. A European study of HLA-B in Stevens-Johnson syndrome and toxic epidermal necrolysis related to five high-risk drugs [J]. Pharmacogenet Genomics , 2008, 18 ( 2 ): 99-107. [ PubMed ] [ Google Scholar ]
41. Ng CY, Yeh YT, Wang CW, et al.. Impact of the HLA-B58: 01 allele and renal impairment on Allopurinol-induced cutaneous adverse reactions [J]. J Invest Dermatol , 2016, 136 ( 7 ): 1373-1381. [ PubMed ] [ Google Scholar ]
42. Park HW, Kim DK, Kim SH, et al.. Efficacy of the HLA-B*58: 01 screening test in preventing allopurinol-induced severe cutaneous adverse reactions in patients with chronic renal insufficiency—A prospective study [J]. J Allergy Clin Immunol Pract , 2019, 7 ( 4 ): 1271-1276. [ PubMed ] [ Google Scholar ]
43. Wang CW, Dao RL, Chung WH. Immunopathogenesis and risk factors for allopurinol severe cutaneous adverse reactions [J]. Curr Opin Allergy Clin Immunol , 2016, 16 ( 4 ): 339-345. [ PubMed ] [ Google Scholar ]
44. Lin CH, Chen JK, Ko TM, et al.. Immunologic basis for allopurinol-induced severe cutaneous adverse reactions: HLA-B*58: 01-restricted activation of drug-specific T cells and molecular interaction [J]. J Allergy Clin Immunol , 2015, 135 ( 4 ): 1063-1065. [ PubMed ] [ Google Scholar ]
45. Fricke-Galindo I, Martínez-Juárez I, Monroy-Jaramillo N, et al.. HLA-A*02: 01: 01/-B*35: 01: 01/-C*04: 01: 01 haplotype associated with lamotrigine-induced maculopapular exanthema in Mexican Mestizo patients [J]. Pharmacogenomics , 2014, 15 ( 15 ): 1881-1891. [ PubMed ] [ Google Scholar ]
46. Lucena MI, Molokhia M, Shen Y, et al.. Susceptibility to amoxicillin-clavulanate-induced liver injury is influenced by multiple HLA class I and II alleles [J]. Gastroenterology , 2011, 141 ( 1 ): 338-347. [ PMC free article ] [ PubMed ] [ Google Scholar ]
47. Yan S, Xiong H, Shao F, et al.. HLA-C*12: 02 is strongly associated with Xuesaitong-induced cutaneous adverse drug reactions [J]. Pharmacogenomics J , 2019, 19 ( 3 ): 277-285. [ PubMed ] [ Google Scholar ]
48. Zhu Q, Zhang Y, Xuan J, et al.. HLA-A*02: 01 allele is associated with tanshinone-induced cutaneous drug reactions in Chinese population [J]. Pharmacogenomics J , 2019, 20 ( 3 ): 408-414. [ PubMed ] [ Google Scholar ]
49. Kaniwa N, Sugiyama E, Saito Y, et al.. Specific HLA types are associated with antiepileptic drug-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in Japanese subjects [J]. Pharmacogenomics , 2013, 14 ( 15 ): 1821-1831. [ PubMed ] [ Google Scholar ]
50. Konvinse KC, Trubiano JA, Pavlos R, et al.. HLA-A*32: 01 is strongly associated with vancomycin-induced drug reaction with eosinophilia and systemic symptoms [J]. J Allergy Clin Immunol , 2019, 144 ( 1 ): 183-192. [ PMC free article ] [ PubMed ] [ Google Scholar ]
51. Zhang FR, Liu H, Irwanto A, et al.. HLA-B*13: 01 and the dapsone hypersensitivity syndrome [J]. N Engl J Med , 2013, 369 ( 17 ): 1620-1628. [ PubMed ] [ Google Scholar ]
52. Chang CC, Ng CC, Too CL, et al.. Association of HLA-B*15: 13 and HLA-B*15: 02 with phenytoin-induced severe cutaneous adverse reactions in a Malay population [J]. Pharmacogenomics J , 2016, 17 ( 2 ): 170-173. [ PubMed ] [ Google Scholar ]
53. Kongpan T, Mahasirimongkol S, Konyoung P, et al.. Candidate HLA genes for prediction of co-trimoxazole-induced severe cutaneous reactions [J]. Pharmacogenet Genomics , 2015, 25 ( 8 ): 402-411. [ PubMed ] [ Google Scholar ]
54. Chen C, Hsiao Y, Wu T, et al.. Risk and association of HLA with oxcarbazepine-induced cutaneous adverse reactions in Asians [J]. Neurology , 2017, 88 ( 1 ): 78-86. [ PubMed ] [ Google Scholar ]
55. Capule F, Tragulpiankit P, Mahasirimongkol S, et al.. Association of carbamazepine-induced Stevens-Johnson syndrome/toxic epidermal necrolysis with the HLA-B75 serotype or HLA-B*15: 21 allele in Filipino patients [J]. Pharmacogenomics J , 2020, 20 ( 3 ): 533-541. [ PubMed ] [ Google Scholar ]
56. Moon J, Kim TJ, Lim JA, et al.. HLA-B*40: 02 and DRB1*04: 03 are risk factors for oxcarbazepine-induced maculopapular eruption [J]. Epilepsia , 2016, 57 ( 11 ): 1879-1886. [ PubMed ] [ Google Scholar ]
57. Yang F, Xuan J, Chen J, et al.. HLA-B*59: 01: a marker for Stevens-Johnson syndrome/toxic epidermal necrolysis caused by methazolamide in Han Chinese [J]. Pharmacogenomics J , 2016, 16 ( 1 ): 83-87. [ PubMed ] [ Google Scholar ]
58. Carr DF, Chaponda M, Jorgensen AL, et al.. Association of human leukocyte antigen alleles and nevirapine hypersensitivity in a Malawian HIV-infected population [J]. Clin Infect Dis , 2013, 56 ( 9 ): 1330-1339. [ PMC free article ] [ PubMed ] [ Google Scholar ]
59. Yuan J, Guo S, Hall D, et al.. Toxicogenomics of nevirapine-associated cutaneous and hepatic adverse events among populations of African, Asian, and European descent [J]. AIDS , 2011, 25 ( 10 ): 1271-1280. [ PMC free article ] [ PubMed ] [ Google Scholar ]
60. Kutszegi N, Yang X, Gezsi A, et al.. HLA-DRB1*07: 01-HLA-DQA1*02: 01-HLA-DQB1*02: 02 haplotype is associated with a high risk of asparaginase hypersensitivity in acute lymphoblastic leukemia [J]. Haematologica , 2017, 102 ( 9 ): 1578- 1586. [ PMC free article ] [ PubMed ] [ Google Scholar ]
61. Hautekeete M, Horsmans Y, van Waeyenberge C, et al.. HLA association of amoxicillin-clavulanate--induced hepatitis [J]. Gastroenterology , 1999, 117 ( 5 ): 1181-1186. [ PubMed ] [ Google Scholar ]
62. Singer JB, Lewitzky S, Leroy E, et al.. A genome-wide study identifies HLA alleles associated with lumiracoxib-related liver injury [J]. Nat Genet , 2010, 42 ( 8 ): 711-714. [ PubMed ] [ Google Scholar ]
63. Kim SH, Saide K, Farrell J, et al.. Characterization of amoxicillin- and clavulanic acid-specific T cells in patients with amoxicillin-clavulanate-induced liver injury [J]. Hepatology , 2015, 62 ( 3 ): 887-899. [ PubMed ] [ Google Scholar ]
64. Sanchez-Gomez FJ, Gonzalez-Morena JM, Vida Y, et al.. Amoxicillin haptenates intracellular proteins that can be transported in exosomes to target cells [J]. Allergy , 2017, 72 ( 3 ): 385-396. [ PubMed ] [ Google Scholar ]
65. Nicoletti P, Aithal GP, Chamberlain TC, et al.. Drug-induced liver injury due to flucloxacillin: Relevance of multiple human leukocyte antigen alleles [J]. Clin Pharmacol Ther , 2019, 106 ( 1 ): 245-253. [ PubMed ] [ Google Scholar ]
66. Petros Z, Kishikawa J, Makonnen E, et al.. HLA-B(*) 57 allele is associated with concomitant anti-tuberculosis and anti-retroviral drugs induced liver toxicity in Ethiopians [J]. Front Pharmacol , 2017, 8 : 90. [ PMC free article ] [ PubMed ] [ Google Scholar ]
67. Yaseen FS, Saide K, Kim SH, et al.. Promiscuous T-cell responses to drugs and drug-haptens [J]. J Allergy Clin Immunol , 2015, 136 ( 2 ): 474-476. [ PubMed ] [ Google Scholar ]
68. Wuillemin N, Adam J, Fontana S, et al.. HLA haplotype determines hapten or p-i T cell reactivity to flucloxacillin [J]. J Immunol , 2013, 190 ( 10 ): 4956-4964. [ PubMed ] [ Google Scholar ]
69. Nicoletti P, Aithal GP, Bjornsson ES, et al.. Association of liver injury from specific drugs, or groups of drugs, with polymorphisms in HLA and other genes in a genome-wide association study [J]. Gastroenterology , 2017, 152 ( 5 ): 1078-1089. [ PMC free article ] [ PubMed ] [ Google Scholar ]
70. Fontana RJ, Cirulli ET, Gu J, et al.. The role of HLA-A*33: 01 in patients with cholestatic hepatitis attributed to terbinafine [J]. J Hepatol , 2018, 69 ( 6 ): 1317-1325. [ PMC free article ] [ PubMed ] [ Google Scholar ]
71. Aithal GP. Of potions, poisons, polygonum, and pre-emptive polymorphism [J]. Hepatology , 2019, 70 ( 1 ): 8-10. [ PubMed ] [ Google Scholar ]
72. 中华中医药学会中成药分会, 中华中医药学会肝胆病分会, 中国药学会临床中药学专业委员会 . 何首乌安全用药指南 [J]. 临床肝胆病杂志 , 2019, 35 ( 12 ): 2687-2693. [ Google Scholar ] Branch of Chinese Patent Medicine, China Association of Chinese Medicine;Branch of Hepatobiliary Diseases . Guidelines for safe use of Polygoni Multiflori Radixl [J]. Journal of Clinical Hepatology , 2019, 35 ( 12 ): 2687-2693. [ Google Scholar ]
73. 李春雨, 李晓菲, 涂灿, 等. 基于内毒素模型的何首乌特异质肝损伤评价 [J]. 药学学报 , 2015, 50 ( 1 ): 28-33. [ PubMed ] [ Google Scholar ] LI Chunyu, LI Xiaofei, TU Can, et al.. The idiosyncratic hepatotoxicity of Polygonum multiflorum based on endotoxin model [J]. Acta Pharmaceutica Sinica , 2015, 50 ( 1 ): 28-33. [ PubMed ] [ Google Scholar ]
74. Hirata K, Takagi H, Yamamoto M, et al.. Ticlopidine-induced hepatotoxicity is associated with specific human leukocyte antigen genomic subtypes in Japanese patients: a preliminary case-control study [J]. Pharmacogenomics J , 2008, 8 ( 1 ): 29-33. [ PubMed ] [ Google Scholar ]
75. Li Y, Phillips E, Dellinger A, et al.. HLA-B*14: 01 and HLA-B*35: 01 are associated with trimethoprim-sulfamethoxazole induced liver injury [J]. Hepatology , 2021, 73 ( 1 ): 268-281. [ PMC free article ] [ PubMed ] [ Google Scholar ]
76. Li C, Rao T, Chen X, et al.. HLA-B*35: 01 Allele is a potential biomarker for predicting polygonum multiflorum-induced liver injury in humans [J]. Hepatology , 2019, 70 ( 1 ): 346-357. [ PubMed ] [ Google Scholar ]
77. Urban TJ, Nicoletti P, Chalasani N, et al.. Minocycline hepatotoxicity: Clinical characterization and identification of HLA-B *35: 02 as a risk factor [J]. J Hepatol , 2017, 67 ( 1 ): 137-144. [ PMC free article ] [ PubMed ] [ Google Scholar ]
78. Bruno CD, Fremd B, Church RJ, et al.. HLA associations with infliximab-induced liver injury [J]. Pharmacogenomics J , 2020, 20 ( 5 ): 681-686. [ PubMed ] [ Google Scholar ]
79. Phillips E, Bartlett J, Sanne I, et al.. Associations between HLA-DRB1*0102, HLA-B*5801, and hepatotoxicity during initiation of nevirapine-containing regimens in South Africa [J]. J Acquir Immune Defic Syndr , 2013, 62 ( 2 ): e55-e57. [ PMC free article ] [ PubMed ] [ Google Scholar ]
80. Kindmark A, Jawaid A, Harbron CG, et al.. Genome-wide pharmacogenetic investigation of a hepatic adverse event without clinical signs of immunopathology suggests an underlying immune pathogenesis [J]. Pharmacogenomics J , 2008, 8 ( 3 ): 186-195. [ PubMed ] [ Google Scholar ]
81. Schaid DJ, Spraggs CF, Mcdonnell SK, et al.. Prospective validation of HLA-DRB1*07: 01 allele carriage as a predictive risk factor for lapatinib-induced liver injury [J]. J Clin Oncol , 2014, 32 ( 22 ): 2296-2303. [ PubMed ] [ Google Scholar ]
82. Keane NM, Pavlos RK, Mckinnon E, et al.. HLA Class I restricted CD8 + and Class II restricted CD4 + T cells are implicated in the pathogenesis of nevirapine hypersensitivity [J]. AIDS , 2014, 28 ( 13 ): 1891-1901. [ PubMed ] [ Google Scholar ]
83. Nicoletti P, Werk AN, Sawle A, et al.. HLA-DRB1*16: 01-DQB1*05: 02 is a novel genetic risk factor for flupirtine-induced liver injury [J]. Pharmacogenet Genomics , 2016, 26 ( 5 ): 218-224. [ PubMed ] [ Google Scholar ]
84. Chen PL, Shih SR, Wang PW, et al.. Genetic determinants of antithyroid drug-induced agranulocytosis by human leukocyte antigen genotyping and genome-wide association study [J]. Nat Commun , 2015, 6 : 7633. [ PMC free article ] [ PubMed ] [ Google Scholar ]
85. Furukawa H, Oka S, Shimada K, et al.. HLA-DRB1*08: 02 is associated with bucillamine-induced proteinuria in Japanese rheumatoid arthritis patients [J]. Biomark Insights , 2014, 9 : 23-28. [ PMC free article ] [ PubMed ] [ Google Scholar ]
86. Furukawa H, Oka S, Shimada K, et al.. HLA-A*31: 01 and methotrexate-induced interstitial lung disease in Japanese rheumatoid arthritis patients: a multidrug hypersensitivity marker? [J]. Ann Rheum Dis , 2013, 72 ( 1 ): 153-155. [ PubMed ] [ Google Scholar ]
87. Wadelius M, Eriksson N, Kreutz R, et al.. Sulfasalazine-induced agranulocytosis is associated with the human leukocyte antigen locus [J]. Clin Pharmacol Ther , 2018, 103 ( 5 ): 843-853. [ PMC free article ] [ PubMed ] [ Google Scholar ]
88. Hallberg P, Eriksson N, Ibañez L, et al.. Genetic variants associated with antithyroid drug-induced agranulocytosis: a genome-wide association study in a European population [J]. Lancet Diabetes Endocrinol , 2016, 4 ( 6 ): 507-516. [ PubMed ] [ Google Scholar ]
89. Saito T, Ikeda M, Mushiroda T, et al.. Pharmacogenomic study of Clozapine-induced agranulocytosis/granulocytopenia in a Japanese population [J]. Biol Psychiatry , 2016, 80 ( 8 ): 636-642. [ PubMed ] [ Google Scholar ]
90. Wilson A, Jansen LE, Rose RV, et al.. HLA-DQA1-HLA-DRB1 polymorphism is a major predictor of azathioprine-induced pancreatitis in patients with inflammatory bowel disease [J]. Aliment Pharmacol Ther , 2018, 47 ( 5 ): 615-620. [ PubMed ] [ Google Scholar ]
91. Mammen AL, Gaudet D, Brisson D, et al.. Increased frequency of DRB1*11: 01 in anti-hydroxymethylglutaryl-coenzyme A reductase-associated autoimmune myopathy [J]. Arthritis Care Res (Hoboken) , 2012, 64 ( 8 ): 1233-1237. [ PMC free article ] [ PubMed ] [ Google Scholar ]
92. Uetrecht J. Idiosyncratic drug reactions: past, present, and future [J]. Chem Res Toxicol , 2008, 21 ( 1 ): 84-92. [ PubMed ] [ Google Scholar ]
93. Nattrass R, Faulkner L, Vocanson M, et al.. Activation of flucloxacillin-specific CD8 + T-cells with the potential to promote hepatocyte cytotoxicity in a mouse model [J]. Toxicol Sci , 2015, 146 ( 1 ): 146-156. [ PubMed ] [ Google Scholar ]
94. Crispe IN. Immune tolerance in liver disease [J]. Hepatology , 2014, 60 ( 6 ): 2109-2117. [ PMC free article ] [ PubMed ] [ Google Scholar ]
95. Schnyder B, Pichler W. Mechanisms of drug-induced allergy [J]. Mayo Clin Proc , 2009, 84 ( 3 ): 268-272. [ PMC free article ] [ PubMed ] [ Google Scholar ]
96. Wei CY, Chung WH, Huang HW, et al.. Direct interaction between HLA-B and carbamazepine activates T cells in patients with Stevens-Johnson syndrome [J]. J Allergy Clin Immunol , 2012, 129 ( 6 ): 1562-1569. [ PubMed ] [ Google Scholar ]
97. White KD, Chung WH, Hung SI, et al.. Evolving models of the immunopathogenesis of T cell-mediated drug allergy: The role of host, pathogens, and drug response [J]. J Allergy Clin Immunol , 2015, 136 ( 2 ): 219-234. [ PMC free article ] [ PubMed ] [ Google Scholar ]
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