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1Academic Journal
Συγγραφείς: I. A. Mazerkina, И. А. Мазеркина
Συνεισφορές: The study reported in this publication was carried out as part of publicly funded research project No. 056-00052-23-00 and was supported by the Scientific Centre for Expert Evaluation of Medicinal Products (R&D public accounting No. 121022400082-4)., Работа выполнена в рамках государственного задания ФГБУ «НЦЭСМП» Минздрава России № 056-00052-23-00 на проведение прикладных научных исследований (номер государственного учета НИР 121022400082-4).
Πηγή: Safety and Risk of Pharmacotherapy; Том 11, № 2 (2023); 204-214 ; Безопасность и риск фармакотерапии; Том 11, № 2 (2023); 204-214 ; 2619-1164 ; 2312-7821
Θεματικοί όροι: человеческий лейкоцитарный антиген, drug-induced hepatotoxicity, iDILI, pathogenesis of idiosyncratic drug-induced hepatotoxicity, immune tolerance, T-cells, signalling pathway activation, genetic risk factors, human leukocyte antigen, HLA, лекарственное повреждение печени, патогенез лекарственной гепатотоксичности, иммунотолерантность, Т-клетки, сигнальные пути активации, генетические факторы риска
Περιγραφή αρχείου: application/pdf
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Trends Immunol. 2017;38(10):768–76. https://doi.org/10.1016/j.it.2017.08.002; Pichler WJ. Pharmacological interaction of drugs with antigen-specific immune receptors: the p-i concept. Curr Opin Allergy Clin Immunol. 2002;2(4):301–5. https://doi.org/10.1097/00130832-200208000-00003; Keisu M, Andersson TB. Drug-induced liver injury in humans: the case of ximelagatran. Handb Exp Pharmacol. 2010;(196):407–18. https://doi.org/10.1007/978-3-642-00663-0_13; Ko TM, Chung WH, Wei CY, Shih HY, Chen JK, Lin CH, Chen YT, Hung SI. Shared and restricted T-cell receptor use is crucial for carbamazepine-induced Stevens-Johnson syndrome. J Allergy Clin Immunol. 2011;128(6):1266–76.e11. https://doi.org/10.1016/j.jaci.2011.08.013; Segovia-Zafra A, Di Zeo-Sánchez DE, López-Gómez C, Pérez-Valdés Z, García-Fuentes E, Andrade RJ, et al. Preclinical models of idiosyncratic drug-induced liver injury (iDILI): moving towards prediction. Acta Pharm Sin B. 2021;11(12):3685–726. https://doi.org/10.1016/j.apsb.2021.11.013; Ogese MO, Jenkins RE, Adair K, Tailor A, Meng X, Faulkner L, et al. Exosomal transport of hepatocyte-derived drug-modified proteins to the immune system. Hepatology. 2019;70(5):1732–49. https://doi.org/10.1002/hep.30701; Cosgrove BD, King BM, Hasan MA, Alexopoulos LG, Farazi PA, Hendriks BS, et al. Synergistic drug-cytokine induction of hepatocellular death as an in vitro approach for the study of inflammation-associated idiosyncratic drug hepatotoxicity. Toxicol Appl Pharmacol. 2009;237(3):317–30. https://doi.org/10.1016/j.taap.2009.04.002; Oda S, Matsuo K, Nakajima A, Yokoi T. A novel cell-based assay for the evaluation of immune- and inflammatory-related gene expression as biomarkers for the risk assessment of drug-induced liver injury. Toxicol Lett. 2016;241:60–70. https://doi.org/10.1016/j.toxlet.2015.10.029; Lowe R, Shirley N, Bleackley M, Dolan S, Shafee T. Transcriptomics technologies. PLoS Comput Biol. 2017;13(5):1005457. https://doi.org/10.1371/journal.pcbi.1005457; De Abrew KN, Overmann GJ, Adams RL, Tiesman JP, Dunavent J, Shan YK, et al. A novel transcriptomics based in vitro method to compare and predict hepatotoxicity based on mode of action. Toxicology. 2015;328:29–39. https://doi.org/10.1016/j.tox.2014.11.008; Ölander M, Wiśniewski JR, Artursson P. Cell-type-resolved proteomic analysis of the human liver. Liver Int. 2020;40(7):1770–80. https://doi.org/10.1111/liv.14452; Cuykx M, Rodrigues RM, Laukens K, Vanhaecke T, Covaci A. In vitro assessment of hepatotoxicity by metabolomics: a review. Arch Toxicol. 2018;92(10):3007–29. https://doi.org/10.1007/s00204-018-2286-9; Sakai C, Iwano S, Yamazaki Y, Ando A, Nakane F, Kouno M, et al. Species differences in the pharmacokinetic parameters of cytochrome P450 probe substrates between experimental animals, such as mice, rats, dogs, monkeys, and microminipigs, and humans. J Drug Metab Toxicol. 2014;5:6. https://doi.org/10.4172/2157-7609.1000173; Metushi IG, Hayes MA, Uetrecht J. Treatment of PD-1(-/-) mice with amodiaquine and anti-CTLA4 leads to liver injury similar to idiosyncratic liver injury in patients. Hepatology. 2015;61(4):1332–42. https://doi.org/10.1002/hep.27549; Chakraborty M, Fullerton AM, Semple K, Chea LS, Proctor WR, Bourdi M, et al. Drug-induced allergic hepatitis develops in mice when myeloid-derived suppressor cells are depleted prior to halothane treatment. Hepatology. 2015;62(2):546–57. https://doi.org/10.1002/hep.27764; Kakuni M, Morita M, Matsuo K, Katoh Y, Nakajima M, Tateno C, Yokoi T. Chimeric mice with a humanized liver as an animal model of troglitazone-induced liver injury. Toxicol Lett. 2012;214(1):9–18. https://doi.org/10.1016/j.toxlet.2012.08.001; Ekdahl A, Weidolf L, Baginski M, Morikawa Y, Thompson RA, Wilson ID. The metabolic fate of fenclozic acid in chimeric mice with a humanized liver. Arch Toxicol. 2018;92(9):2819–28. https://doi.org/10.1007/s00204-018-2274-0; Song B, Aoki S, Liu C, Susukida T, Ito K. An animal model of abacavir-induced HLA-mediated liver injury. Toxicol Sci. 2018;162(2):713–23. https://doi.org/10.1093/toxsci/kfy001; McGill MR, Jaeschke H. Animal models of drug-induced liver injury. Biochim Biophys Acta Mol Basis Dis. 2019;1865(5):1031–9. https://doi.org/10.1016/j.bbadis.2018.08.037; Stephens C, Lucena MI, Andrade RJ. Genetic risk factors in the development of idiosyncratic drug-induced liver injury. Expert Opin Drug Metab Toxicol. 2021;17(2):153–69. https://doi.org/10.1080/17425255.2021.1854726; Pachkoria K, Lucena MI, Ruiz-Cabello F, Crespo E, Cabello MR, Andrade RJ. Genetic polymorphisms of CYP2C9 and CYP2C19 are not related to drug-induced idiosyncratic liver injury (DILI). Br J Pharmacol. 2007;150(6):808–15. https://doi.org/10.1038/sj.bjp.0707122; Zhao M, Zhang T, Li G, Qiu F, Sun Y, Zhao L. Associations of CYP2C9 and CYP2A6 polymorphisms with the concentrations of valproate and its hepatotoxin metabolites and valproate-induced hepatotoxicity. Basic Clin Pharmacol Toxicol. 2017;121(2):138–43. https://doi.org/10.1111/bcpt.12776; Yimer G, Amogne W, Habtewold A, Makonnen E, Ueda N, Suda A, et al. High plasma efavirenz level and CYP2B6*6 are associated with efavirenz-based HAART-induced liver injury in the treatment of naïve HIV patients from Ethiopia: a prospective cohort study. Pharmacogenomics J. 2012;12(6):499–506. https://doi.org/10.1038/tpj.2011.34; Hu X, Zhang M, Bai H, Wu L, Chen Y, Ding L, et al. Antituberculosis drug-induced adverse events in the liver, kidneys, and blood: clinical profiles and pharmacogenetic predictors. Clin Pharmacol Ther. 2018;104(2):326–34. https://doi.org/10.1002/cpt.924; Daly AK, Aithal GP, Leathart JB, Swainsbury RA, Dang TS, Day CP. Genetic susceptibility to diclofenac-induced hepatotoxicity: contribution of UGT2B7, CYP2C8, and ABCC2 genotypes. Gastroenterology. 2007;132(1):272–81. https://doi.org/10.1053/j.gastro.2006.11.023; Wattanapokayakit S, Mushiroda T, Yanai H, Wichukchinda N, Chuchottawon C, Nedsuwan S, et al. NAT2 slow acetylator associated with anti-tuberculosis drug-induced liver injury in Thai patients. Int J Tuberc Lung Dis. 2016;20(10):1364–9. https://doi.org/10.5588/ijtld.15.0310; Sharma SK, Jha BK, Sharma A, Sreenivas V, Upadhyay V, Jaisinghani C, et al. Genetic polymorphisms of N-acetyltransferase 2 & susceptibility to antituberculosis drug-induced hepatotoxicity. Indian J Med Res. 2016;144(6):924–8. https://doi.org/10.4103/ijmr.IJMR_684_14; Du H, Chen X, Fang Y, Yan O, Xu H, Li L, et al. Slow N-acetyltransferase 2 genotype contributes to anti-tuberculosis drug-induced hepatotoxicity: a meta-analysis. Mol Biol Rep. 2013;40(5):3591–6. https://doi.org/10.1007/s11033-012-2433-y; Suvichapanich S, Fukunaga K, Zahroh H, Mushiroda T, Mahasirimongkol S, Toyo-Oka L, et al. NAT2 ultra-slow acetylator and risk of anti-tuberculosis drug-induced liver injury: a genotype-based meta-analysis. Pharmacogenet Genomics. 2018;28(7):167–76. https://doi.org/10.1097/FPC.0000000000000339; Zhang M, Wang S, Wilffert B, Tong R, van Soolingen D, van den Hof S, Alffenaar JW. The association between the NAT2 genetic polymorphisms and risk of DILI during anti-TB treatment: a systematic review and meta-analysis. Br J Clin Pharmacol. 2018;84(12):2747–60. https://doi.org/10.1111/bcp.13722; Li YJ, Phillips EJ, Dellinger A, Nicoletti P, Schutte R, Li D, et al. Human leukocyte antigen B*14:01 and B*35:01 are associated with trimethoprim-sulfamethoxazole induced liver injury. Hepatology. 2021;73(1):268–81. https://doi.org/10.1002/hep.31258; Hirata K, Takagi H, Yamamoto M, Matsumoto T, Nishiya T, Mori K, et al. Ticlopidine-induced hepatotoxicity is associated with specific human leukocyte antigen genomic subtypes in Japanese patients: a preliminary case-control study. Pharmacogenomics J. 2008;8(1):29–33. https://doi.org/10.1038/sj.tpj.6500442; Li C, Rao T, Chen X, Zou Z, Wei A, Tang J, et al. HLA-B*35:01 allele is a potential biomarker for predicting Polygonum multiflorum-induced liver injury in humans. Hepatology. 2019;70(1):346–57. https://doi.org/10.1002/hep.30660; Yang WN, Pang LL, Zhou JY, Qiu YW, Miao L, Wang SY, et al. Single-nucleotide polymorphisms of HLA and Polygonum multiflorum-induced liver injury in the Han Chinese population. World J Gastroenterol. 2020;26(12):1329–39. https://doi.org/10.3748/wjg.v26.i12.1329; O’Donohue J, Oien KA, Donaldson P, Underhill J, Clare M, MacSween RN, Mills PR. Co-amoxiclav jaundice: clinical and histological features and HLA class II association. Gut. 2000;47(5):717–20. https://doi.org/10.1136/gut.47.5.717; Aithal GP, Ramsay L, Daly AK, Sonchit N, Lea thart JB, Alexander G, et al. Hepatic adducts, circulating antibodies, and cytokine polymorphisms in patients with diclofenac hepatotoxicity. Hepatology. 2004;39(5):1430–40. https://doi.org/10.1002/hep.20205; Uffelmann E, Huang QQ, Munung NS, Vries J, Okada Y, Martin AR, et al. Genome-wide association studies. Nat Rev Methods Primers. 2021;(1):59. https://doi.org/10.1038/s43586-021-00056-9; Suvichapanich S, Wattanapokayakit S, Mushiroda T, Yanai H, Chuchottawon C, Kantima T, et al. Genomewide association study confirming the association of NAT2 with susceptibility to antituberculosis drug-induced liver injury in Thai patients. Antimicrob Agents Chemother. 2019;63(8):e02692–18. https://doi.org/10.1128/AAC.02692-18; Lucena MI, Molokhia M, Shen Y, Urban TJ, Aithal GP, Andrade RJ, et al. Susceptibility to amoxicillin-clavulanate-induced liver injury is influenced by multiple HLA class I and II alleles. Gastroenterology. 2011;141(1):338–47. https://doi.org/10.1053/j.gastro.2011.04.001; Nicoletti P, Barrett S, McEvoy L, Daly AK, Aithal G, Lucena MI, et al. Shared genetic risk factors across carbamazepine-induced hypersensitivity reactions. Clin Pharmacol Ther. 2019;106(5):1028–36. https://doi.org/10.1002/cpt.1493; Nicoletti P, Aithal GP, Bjornsson ES, Andrade RJ, Sawle A, Arrese M, 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. Gastroenterology. 2017;152(5):1078–89. https://doi.org/10.1053/j.gastro.2016.12.016; Urban TJ, Nicoletti P, Chalasani N, Serrano J, Stolz A, Daly AK, et al. Minocycline hepatotoxicity: clinical characterization and identification of HLA-B*35:02 as a risk factor. J Hepatol. 2017;67(1):137–44. https://doi.org/10.1016/j.jhep.2017.03.010; Bruno CD, Fremd B, Church RJ, Daly AK, Aithal GP, Björnsson ES, et al. HLA associations with infliximab-induced liver injury. Pharmacogenomics J. 2020;20(5):681–6. https://doi.org/10.1038/s41397-020-0159-0; Daly AK, Donaldson PT, Bhatnagar P, Shen Y, Pe’er I, Floratos A, et al. HLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin. Nat Genet. 2009;41(7):816–9. https://doi.org/10.1038/ng.379; Nicoletti P, Aithal GP, Chamberlain TC, Coulthard S, Alshabeeb M, Grove JI, et al. Drug-induced liver injury due to flucloxacillin: relevance of multiple human leukocyte antigen alleles. Clin Pharmacol Ther. 2019;106(1):245–53. https://doi.org/10.1002/cpt.1375; Kindmark A, Jawaid A, Harbron CG, Barratt BJ, Bengtsson OF, Andersson TB, et al. Genome-wide pharmacogenetic investigation of a hepatic adverse event without clinical signs of immunopathology suggests an underlying immune pathogenesis. Pharmacogenomics J. 2008;8(3):186–95. https://doi.org/10.1038/sj.tpj.6500458; Spraggs CF, Budde LR, Briley LP, Bing N, Cox CJ, King KS, et al. HLA-DQA1*02:01 is a major risk factor for lapatinib-induced hepatotoxicity in women with advanced breast cancer. J Clin Oncol. 2011;29(6):667–73. https://doi.org/10.1200/JCO.2010.31.3197; Parham LR, Briley LP, Li L, Shen J, Newcombe PJ, King KS, et al. Comprehensive genome-wide evaluation of lapatinib-induced liver injury yields a single genetic signal centered on known risk allele HLA-DRB1*07:01. Pharmacogenomics J. 2016;16(2):180–5. https://doi.org/10.1038/tpj.2015.40; Singer JB, Lewitzky S, Leroy E, Yang F, Zhao X, Klickstein L, et al. A genome-wide study identifies HLA alleles associated with lumiracoxib-related liver injury. Nat Genet. 2010;42(8):711–4. https://doi.org/10.1038/ng.632; Nicoletti P, Werk AN, Sawle A, Shen Y, Urban TJ, Coulthard SA, et al. HLA-DRB1*16: 01-DQB1*05: 02 is a novel genetic risk factor for flupirtine-induced liver injury. Pharmacogenet Genomics. 2016;26(5):218–24. https://doi.org/10.1097/FPC.0000000000000209; Cirulli ET, Nicoletti P, Abramson K, Andrade RJ, Bjornsson ES, Chalasani N, et al. A missense variant in PTPN22 is a risk factor for drug-induced liver injury. Gastroenterology. 2019;156(6):1707–1716.e2. https://doi.org/10.1053/j.gastro.2019.01.034; Zhang X, Yu Y, Bai B, Wang T, Zhao J, Zhang N, et al. PTPN22 interacts with EB1 to regulate T-cell receptor signaling. FASEB J. 2020;34(7):8959–74. https://doi.org/10.1096/fj.201902811RR; Alfirevic A, Pirmohamed M. Predictive genetic testing for drug-induced liver injury: considerations of clinical utility. 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2Academic Journal
Συγγραφείς: Резниченко, Л., Воробиевская, С., Пензева, М.
Θεματικοί όροι: ИММУНОТОЛЕРАНТНОСТЬ, АНТИГЕН, АНТИТЕЛО, ПЛОД, ПЛАЦЕНТА, СВИНОВОДЧЕСКОЕ ХОЗЯЙСТВО, ВАКЦИНАЦИЯ, СВИНКИ, ПАРВОВИРУСНАЯ БОЛЕЗНЬ, ЦИРКОВИРУСНАЯ БОЛЕЗНЬ СВИНЕЙ, РЕПРОДУКТИВНО-РЕСПИРАТОРНЫЙ СИНДРОМ СВИНЕЙ
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3Academic Journal
Συγγραφείς: Дмитриев, Анатолий
Θεματικοί όροι: ИНФЕКЦИЯ, ПЛОД, ПОТОМСТВО, ФАКТОРЫ РИСКА, ВИРУС ЛЕЙКОЗА КРУПНОГО РОГАТОГО СКОТА, РОГАТЫЙ СКОТ, ИММУНОДЕФИЦИТ, ИММУННАЯ СИСТЕМА, ИММУНОТОЛЕРАНТНОСТЬ
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4Academic Journal
Συγγραφείς: Одинак, М., Чирский, B., Бисага, Г., БАЛДУЕВА S И.А., МОИСЕЕНКО Г В.М., НЕХАЕВА Г Т.П., Калинина, Н., Давыдова, Н., Бычкова, Н., Чумаш, К.
Θεματικοί όροι: РАССЕЯННЫЙ СКЛЕРОЗ, ДЕНДРИТНЫЕ КЛЕТКИ, ИММУНОТОЛЕРАНТНОСТЬ
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5Academic Journal
Πηγή: Ученые записки Казанской государственной академии ветеринарной медицины им. Н.Э. Баумана.
Θεματικοί όροι: ИММУНОТОЛЕРАНТНОСТЬ, АНТИГЕН, АНТИТЕЛО, ПЛОД, ПЛАЦЕНТА, СВИНОВОДЧЕСКОЕ ХОЗЯЙСТВО, ВАКЦИНАЦИЯ, СВИНКИ, ПАРВОВИРУСНАЯ БОЛЕЗНЬ, ЦИРКОВИРУСНАЯ БОЛЕЗНЬ СВИНЕЙ, РЕПРОДУКТИВНО-РЕСПИРАТОРНЫЙ СИНДРОМ СВИНЕЙ, 3. Good health
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6Academic Journal
Πηγή: Ветеринарная патология.
Περιγραφή αρχείου: text/html
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7Academic Journal
Συγγραφείς: Чирский, B., БАЛДУЕВА S И.А.
Πηγή: Гены и клетки.
Θεματικοί όροι: РАССЕЯННЫЙ СКЛЕРОЗ, ДЕНДРИТНЫЕ КЛЕТКИ, ИММУНОТОЛЕРАНТНОСТЬ, 3. Good health
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8Academic Journal
Συγγραφείς: Pavlunina M.M., Mazurchik N.V., Ogurtsov P.P.
Πηγή: Вестник последипломного медицинского образования
Θεματικοί όροι: хронический гепатит B, иммунотолерантность, гепатоцеллюлярная карцинома, острый вирусный гепатит, диагностика, лечение, прогноз, chronic hepatitis B, immune tolerance, hepatocellular carcinoma, acute viral hepatitis, diagnosis, treatment, prognosis
Διαθεσιμότητα: https://repository.rudn.ru/records/article/record/51984/