Обоснование. Псориаз – это хроническое воспалительное аутоиммунное заболевание, характеризующееся чрезмерно аберрантной гиперпролиферацией кератиноцитов. Патогенез псориаза сложен, и точный механизм, несмотря на многочисленные исследования, до сих пор остается неясным. Сложные генетические связи играют важную роль в патогенезе этого дерматологического заболевания. В развитии псориаза задействовано большое количество генов, также ассоциированных с другими заболеваниями. Широкий спектр наблюдаемых у пациентов с псориазом коморбидных состояний зачастую весьма затрудняет терапию дерматоза. Понимание роли некоторых генов в патогенезе псориатического процесса позволит разработать более эффективное целевое лечение, направленное на блокирование соответствующих воспалительных сигнальных путей и молекул. Цель. Проанализировать и систематизировать основные генетические и биологические маркеры псориаза. Материалы и методы. В исследование включены исследовательские статьи, посвященные генетическому анализу псориаза. Использовались реферативные базы ResNet, PubMed и eLibrary. Результаты и обсуждение. В результате проведенного детального анализа литературных источников, посвященных псориатической болезни, определен круг основных генетических и биологических маркеров. Уделено внимание роли и влиянию однонуклеотидных полиморфизмов, которые позволяют установить четкую ассоциацию ряда генов, задействованных в развитии псориаза. Отдельно рассматривались гены с измененной экспрессией при псориатическом процессе. Заключение. Выявленные биомаркеры могут применяться в направленной биологической терапии псориаза с использованием биологических модуляторов, которые блокируют передачу сигналов.
Background. Psoriasis is a chronic inflammatory autoimmune disease characterized by an excessively aberrant hyperproliferation of keratinocytes. The pathogenesis of psoriasis is complex, and the exact mechanism, despite numerous studies, is still unclear. Complex genetic relationships play an important role in the pathogenesis of this skin disease. A large number of genes that are also associated with other diseases are involved in the development of psoriasis. The variety of comorbidities in patients with psoriasis often present challenges to the treatment for dermatosis. Understanding the role of certain genes in the pathogenesis of psoriasis will contribute the development of more effective targeted therapy aimed at blocking the corresponding inflammatory signaling pathways and molecules. Aim. To analyze and systematize the basic genetic and biological markers of psoriasis. Materials and methods. The study included research articles on the genetic analysis of psoriasis. The ResNet, PubMed and eLibrary databases were used.
Results and discussion. Basic genetic and biological markers were identified by analysis of literature sources devoted to psoriasis. Attention is paid to the role and effects of single nucleotide polymorphisms, which make it possible to establish a clear association of a number of genes involved in the development of psoriasis. Genes with altered expression in the psoriatic process were considered separately. Conclusion. The identified biomarkers can be used in targeted biological therapy of psoriasis using biological modulators that block signaling.
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DOI:10.1007/s00403-011-1129-9
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________________________________________________
1. Seldin MF. The Genetics of Human Autoimmune Disease: A Perspective on Progress in the Field and Future Directions. J Autoimmun. 2015;64:1-12. DOI:10.1016/j.jaut.2015.08.015
2. Duffin KC, Chandran V, Gladman DD, et al. Genetics of psoriasis and psoriatic arthritis: update and future direction. J Rheumatol. 2008;35:1449-53. PMID: 18609743
3. Nesterova AP, Klimov EA, Zharkova M, et al. Diseases of the skin and subcutaneous tissue. In Disease Pathways. Elsevier, 2020; p. 493-532. DOI:10.1016/B978-0-12-817086-1.00011-7
4. Nesterova AP, Yuryev A, Klimov EA, et al. Disease Pathways: An atlas of human disease signaling pathways. 1st ed. Elsevier: Waltham, 2019. DOI:10.1016/C2018-0-00586-1
5. Sobolev VV, Mezentsev AV, Ziganshin RH, et al. LC-MS/MS Analysis of Lesional and Normally Looking Psoriatic Skin Reveals Significant Changes in Protein Metabolism and RNA Processing. PLoS One. 2021;16:e0240956. DOI:10.1371/journal.pone.0240956
6. Farber EM, Nall L. The Natural History of Psoriasis in 5,600 Patients. Dermatology. 1974;148:1-18. DOI:10.1159/000251595
7. Allione A, Marcon F, Fiorito G, et al. Novel Epigenetic Changes Unveiled by Monozygotic Twins Discordant for Smoking Habits. PloS One. 2015;10:e0128265. DOI:10.1371/journal.pone.0128265
8. Park J-H, Wacholder S, Gail MH, et al. Estimation of Effect Size Distribution from Genome-Wide Association Studies and Implications for Future Discoveries. Nat Genet. 2010;42:570-5. DOI:10.1038/ng.610
9. Nair RP, Stuart PE, Nistor I, et al. Sequence and Haplotype Analysis Supports HLA-C as the Psoriasis Susceptibility 1 Gene. Am J Hum Genet. 2006;78:827-51. DOI:10.1086/503821
10. Hız MM, Kılıç S, Oymak S, et al. Psoriasis and Genetics. IntechOpen: Rijeka, 2017. DOI:10.5772/intechopen.68344
11. De Cid R, Riveira-Munoz E, Zeeuwen PLJM, et al. Deletion of the Late cornified envelope LCE3B and LCE3C genes as a susceptibility factor for psoriasis. Nat Genet. 2009;41:211-5. DOI:10.1038/ng.313
12. Coto-Segura P, Coto E, Mas-Vidal A, et al. Influence of Endothelial Nitric Oxide Synthase Polymorphisms in Psoriasis Risk. Arch Dermatol Res. 2011;303:445-9.
DOI:10.1007/s00403-011-1129-9
13. Fu L, Zhao Y, Lu J, et al. Functional Single Nucleotide Polymorphism-1026C/A of Inducible Nitric Oxide Synthase Gene with Increased YY1-Binding Affinity Is Associated with Hypertension in a Chinese Han Population. J Hypertens. 2009;27:991-1000. DOI:10.1097/hjh.0b013e3283294bec
14. Klimov EА, Tretiakov AV, Gapanovich ES, et al. Evaluation of the role of polymorphic variants of no-synthases genes of in pathogenesis of psoriasis. Mol Meditsina Mol Med. 2018;16. DOI:10.29296/24999490-2018-04-11
15. Klimov E, Tretiakov A, Gapanovich E, et al. Assessment of the role of NO synthase genes polymorphisms in the pathogenesis of psoriasis. J Adv Med Med Res. 2018;26:1-6. DOI:10.9734/JAMMR/2018/41039
16. Sobolev V, Sakaniya L, Tretiakov A, et al. Association of GA Genotype of SNP Rs4680 in COMT Gene with Psoriasis. Arch Dermatol Res. 2019;311:309-15. DOI:10.1007/s00403-019-01904-1
17. Sakaniya LR, Tretiakov AV, Shevtsova AA, et al. DBH gene polymorphism in psoriasis patients. Mol Meditsina Mol Med. 2019;17. DOI:10.29296/24999490-2019-04-09
18. Klimov E, Tretiakov A, Rudko O, et al. Psychodermatology: a molecular link between psoriasis and anxiety disorder. Acta Dermatovenerol Alp Pannonica Adriat. 2018;27. DOI:10.15570/actaapa.2018.38
19. Sobolev V, Klimov E, Tretiakov A, et al. 218 polymorphism of dopamine related genes in the light of psychodermatology: association with psoriasis. J Invest Dermatol. 2017;137:S230. DOI:10.1016/j.jid.2017.07.215
20. Sobolev VV, Tret'iakov AV, Rud'ko OI, et al. Psikhodermatologiia: molekuliarnaia obshchnost' psoriaza i trevozhnogo rasstroistva. Effektivnaia farmakoterapiia. 2017;15:10-5 (in Russian).
21. Danilin IE, Niewozinska ZA, Tretiakov AV, et al. Analysis of the relationship between skin and emotional disorders in patients with psoriasis. Bulletin of Neurology, Psychiatry and Neurosurgery. 2020;11 (in Russian). DOI: 10.33920/med-01-2011-02
22. Nair RP, Duffin KC, Helms C, et al. Genome-Wide Scan Reveals Association of Psoriasis with IL-23 and NF-KappaB Pathways. Nat Genet. 2009;41:199-204. DOI:10.1038/ng.311
23. Di Meglio P, Di Cesare A, Laggner U, et al. The IL23R R381Q Gene Variant Protects against Immune-Mediated Diseases by Impairing IL-23-Induced Th17 Effector Response in Humans. PLoS ONE. 2011;6:e17160. DOI: 10.1371/journal.pone.0017160
24. Sobolev VV, Tret'iakov AV, Shevtsova AA, et al, Sviaz' mezhdu odnonukleotidnoi zamenoi T>C v gene MIR22 i razvitiem psoriaza. Effektivnaia farmakoterapiia. 2018;34:18-20 (in Russian).
25. Johansen C, Usher PA, Kjellerup RB, et al. Characterization of the Interleukin-17 Isoforms and receptors in lesional psoriatic skin. Br J Dermatol. 2009;160:319-24.
DOI:10.1111/j.1365-2133.2008.08902.x
26. Sobolev VV, Sautin ME, Piruzian ES, et al. IL-17 gene expression levels in atherosclerosis and psoriasis. Prime. 2015;5:34-8. Available at: https://www.prime-journal.com/il-17-gene-expression-levels-in-atherosclerosis-and-psoriasis/ Accessed: 13.08.2021.
27. Isailovic N, Daigo K, Mantovan A, Selmi C. Interleukin-17 and innate immunity in infections and chronic inflammation. J Autoimmun. 2015;60:1-11. DOI:10.1016/j.jaut.2015.04.006
28. Lai Y, Li D, Li C, et al. The Antimicrobial protein REG3A regulates keratinocyte proliferation and differentiation after skin injury. Immunity. 2012;37:74-84. DOI:10.1016/j.immuni.2012.04.010
29. Sobolev VV, Denisova EV, Korsunskaia IM. Izmenenie ekspressii gena S100A8 pod vozdeistviem lazernogo izlucheniia nizkoi intensivnosti u bol'nykh psoriazom. Effektivnaia farmakoterapiia. 2021;17:14-6 (in Russian). DOI:10.33978/2307-3586-2021-17-1-14-16
30. Il'ina SA, Zolotarenko AD, Piruzian AL, et al. Ekspressiia genov S100A8 i S100A9 v porazhennoi psoriaticheskim protsessom kozhe. Tekhnologii zhivykh sistem. 2010;7:45-51 (in Russian).
31. Ramirez-Carrozzi V, Sambandam A, Luis E, et al. IL-17C Regulates the innate immune function of epithelial cells in an autocrine manner. Nat Immunol. 2011;12:1159-66. DOI:10.1038/ni.2156
32. Kanda N, Koike S, Watanabe S. IL-17 Suppresses TNF-Alpha-Induced CCL27 Production through Induction of COX-2 in Human Keratinocytes. J Allergy Clin Immunol. 2005;116:1144-50. DOI:10.1016/j.jaci.2005.08.014
33. Cargill M, Schrodi SJ, Chang M, et al. A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes. Am J Hum Genet. 2007;80:273-90. DOI:10.1086/511051
34. Johnson-Huang LM, Suárez-Fariñas M, Pierson KC, et al. A single intradermal injection of IFN-γ induces an inflammatory state in both non-lesional psoriatic and healthy skin. J Invest Dermatol. 2012;132:1177-87. DOI:10.1038/jid.2011.458
35. Sobolev VV, Denisova EV, Korsunskaya IM. Alteration of STAT3 gene expression in psoriasis treatment. Medical Council. 2020;12:71-4 (in Russian). DOI:10.21518/2079-701X-2020-12-71-74
36. Madonna S, Scarponi C, Sestito R, et al. The IFN-gamma-dependent suppressor of cytokine signaling 1 promoter activity is positively regulated by IFN regulatory factor-1 and Sp1 but repressed by growth factor independence-1b and krüppel-like factor-4, and it is dysregulated in psoriatic keratinocytes. J Immunol. 2010;185:2467-81. DOI:10.4049/jimmunol.1001426
37. Abdallah MA, Abdel-Hamid MF, Kotb AM, Mabrouk EA. Serum interferon-gamma is a psoriasis severity and prognostic marker. Cutis. 2009;84:163-8. PMID: 19842576
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1 ГБУЗ «Московский научно-практический центр дерматовенерологии и косметологии» Департамента здравоохранения г. Москвы, Москва, Россия;
2 ФГБУН «Центр теоретических проблем физико-химической фармакологии» РАН, Москва, Россия;
3 ФГАОУ ВО «Российский университет дружбы народов», Москва, Россия;
4 ФГАОУ ВО «Российский национальный исследовательский медицинский университет им. Н.И. Пирогова» Минздрава России, Москва, Россия
*dr.melnichenko@gmail.com
________________________________________________
Olga O. Melnichenko*1, Elena V. Denisova1,2, Olga V. Zhukova1,3, Nikolay N. Potekaev1,4
1 Moscow Scientific and Practical Center of Dermatology, Venereology and Cosmetology, Moscow, Russia;
2 Center for Theoretical Problems of Physicochemical Pharmacology, Moscow, Russia;
3 Peoples’ Friendship University of Russia (RUDN University), Moscow, Russia;
4 Pirogov Russian National Research Medical University, Moscow, Russia
*dr.melnichenko@gmail.com