mimmunМедицинская иммунологияMedical Immunology (Russia)1563-06252313-741XSPb RAACI10.15789/1563-0625-GGI-2937mimmun-2937Research ArticleОРИГИНАЛЬНЫЕ СТАТЬИORIGINAL ARTICLESГен-генные взаимодействия цитокинов и C-реактивного белка при псориазе у жителей Кемеровской областиGene-gene interactions of cytokines and C-reactive protein in psoriasis in residents of Kemerovo regionРомановаЕ. Л.RomanovaE. L.

Романова Елизавета Леонидовна - аспирантка кафедры генетики и фундаментальной медицины

650000, г. Кемерово, ул. Красная, 6

Тел.: 8 (3842) 58-01-66

Elizaveta L. Romanova, Postgraduate Student, Department of Genetics and Fundamental Medicine

6 Krasnaya St Kemerovo 650000

Phone: +7 (3842) 58-01-66

Rom11elizaveta@yandex.ruhttps://orcid.org/0000-0002-8785-7896ШабалдинА. В.ShabaldinA. V.

Шабалдин А.В. – д.м.н., доцент, профессор кафедры генетики и фундаментальной медицины

г. Кемерово

Shabaldin A.V., PhD, MD (Medicine), Associate Professor, Professor, Department of Genetics and Fundamental Medicine

Kemerovo

weit2007@yandex.ruБеловЕ. Г.BelovE. G.

Белов Е.Г. – главный врач

г. Кемерово

Belov E.G., Chief Physician

Kemerovo

epid1720@mail.ruСтригаЛ. В.StrigaL. V.

Стрига Л.В. – к.м.н., заместитель главного врача по медицинской части

г. Кемерово

Striga L.V., PhD (Medicine), Deputy Chief Physician for Medicine

Kemerovo

asya-kemerovo2012@yandex.ruhttps://orcid.org/0000-0002-6987-8247ЯковлеваА. А.YakovlevaA. A.

Яковлева А.А. – инженер кафедры генетики и фундаментальной медицины

г. Кемерово

Yakovleva A.A., Engineer, Department of Genetics and Fundamental Medicine

Kemerovo

asya-kemerovo2012@yandex.ruШевченкоЕ. А.ShevchenkoE. A.

Шеченко Е.А. – заведующая микологическим отделением 

г. Кемерово

Shevchenko E.A., Head, Mycological Department No. 1

Kemerovo

e-shevche@rambler.ruШабалдинаЕ. В.ShabaldinaE. V.

Шабалдина Е.В. – д.м.н., доцент, заведующая кафедрой оториноларингологии

г. Кемерово

Shabaldina E.V., PhD, MD (Medicine), Associate Professor, Head, Department of Otorhinolaryngology

Kemerovo

weit2007@yandex.ruФГБОУ ВО «Кемеровский государственный университет»РоссияKemerovo State UniversityRussian FederationГБУЗ «Кузбасский клинический кожно-венерологический диспансер»РоссияKuzbass Clinical Skin and Venereological DispensaryRussian FederationФГБОУ ВО «Кемеровский государственный медицинский университет»РоссияKemerovo State Medical UniversityRussian Federation2025080120252718796Copyright © Романова Е.Л., Шабалдин А.В., Белов Е.Г., Стрига Л.В., Яковлева А.А., Шевченко Е.А., Шабалдина Е.В., 20252025Романова Е.Л., Шабалдин А.В., Белов Е.Г., Стрига Л.В., Яковлева А.А., Шевченко Е.А., Шабалдина Е.В.Romanova E.L., Shabaldin A.V., Belov E.G., Striga L.V., Yakovleva A.A., Shevchenko E.A., Shabaldina E.V.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.mimmun.ru/mimmun/article/view/2937

Псориаз является наиболее распространенным воспалительным заболеванием кожи, которым страдает в среднем 2-4% населения Земли. Согласно современным представлениям, псориаз является мультифакториальным заболеванием, возникающим у генетически предрасположенных лиц под воздействием различных факторов окружающей среды, которые запускают нарушение иммунного ответа с серией сложных воспалительных каскадов. Заболевание инициируется и поддерживается взаимным взаимодействием клеток врожденного и адаптивного иммунитета, прежде всего дендритных клеток, Т-лимфоцитов и кератиноцитов, ведущая роль которых на разных стадиях заболевания чередуется и заключается в основном в IL-23/Th17-пути. На сегодняшний день описано множество полиморфизмов генов (SNP), связанных с развитием псориаза. Для понимания патофизиологии псориаза, как сложного аутовоспалительного заболевания, представляется интересным изучение межгенных взаимодействий полиморфных вариантов генов цитокинов и С-реактивного белка в отношении риска развития псориаза. Цель работы – изучить межгенные взаимодействия полиморфных вариантов генов IL1β (rs16944), IL6 (rs1554606), IL8 (rs2227306), IL10 (rs1800896), TNFα (rs361525), СRP (rs1205) связанных с риском развития псориаза у жителей Кемеровской области. Обследовано 175 пациентов с обыкновенным папулезно-бляшечным псориазом, с прогрессирующим течением в средней степени тяжести. Контрольная группа (n = 155) сформирована из условно-здоровых доноров того же возрастного интервала. Генотипирование осуществляли с помощью метода ПЦР с использованием TaqMan зондов (Thermo Fisher Scientific, США) на детектирующем амплификаторе ViiATM 7 Real-Time PCR System (Life Technologies, США) следующих полиморфных вариантов генов: IL1β (rs16944), IL6 (rs1554606), IL8 (rs2227306), IL10 (rs1800896), TNFα (rs361525), СRP (rs1205). Анализ межгенных взаимодействий осуществляли при помощи метода сокращения многофакторной размерности (Multifactor Dimensionality Reduction, MDR). Установлено, что детерминирование обыкновенного папулезно-бляшечного псориаза связано как с отдельными полиморфными вариантами генов цитокинов и С-реактивного белка, так и ген-генными взаимодействиями. Для отдельных полиморфных вариантов генов сила (% энтропии) ассоциации с обыкновенным папулезно-бляшечным псориазом была следующая: TNFα_rs361525 (16,99% энтропии), IL1β_rs16944 (6,40% энтропии), CRP_rs1205 (2,55% энтропии), IL6_rs1554606 (1,11% энтропии), IL10_rs1800896 (0,57% энтропии), IL8_rs2227306 (0,30% энтропии). Выявлено, что выраженным синергизмом обладали IL6 (rs1554606) и IL8 (rs2227306); умеренным синергизмом CRP (rs1205) и IL10 (rs1800896) и выраженным антагонизмом IL1β (rs16944) и TNFα (rs361525).

Psoriasis is the most common inflammatory skin disease, affecting on average 2-4% of the world’s population. Currently, psoriasis is considered a multifactorial disease occurring in genetically predisposed individuals under the influence of various environmental factors that trigger a disrupted immune response via complex inflammatory cascades. The disease is initiated and maintained by the mutual interaction of cells of innate and adaptive immunity, primarily, dendritic cells, T lymphocytes and keratinocytes. Their leading role may alternate at different stages of the disease and proceeds, mainly, at the IL-23/Th17 pathway. To date, many gene polymorphisms (SNPs) associated with the development of psoriasis have been described. To understand the pathophysiology of psoriasis as a complex autoinflammatory disease, it seems interesting to study the intergenic interactions between polymorphic gene variants of cytokines and C-reactive protein related to the risk of psoriasis development. The aim of our study was to investigate intergenic interactions of polymorphic variants of IL1β (rs16944), IL6 (rs1554606), IL8 (rs2227306), IL10 (rs1800896), TNFα (rs361525), CRP (rs1205) genes associated with altered risk of psoriasis development among the Kemerovo Region residents. We examined 175 patients with ordinary papular plaque psoriasis of moderate severity, with progressive course of the disorder. The control group (n = 155) was recruited from conditionally healthy, age-matched donors. Genotyping was performed by PCR using TaqMan probes (Thermo Fisher Scientific, USA), by means of the detection amplifier ViiATM 7 Real-Time PCR System (Life Technologies, USA), for the following polymorphic variants of genes: IL1β (rs16944), IL6 (rs1554606), IL8 (rs2227306), IL10 (rs1800896), TNFα (rs361525), CRP (rs1205). Intergenic interactions were analyzed using Multifactor Dimensionality Reduction (MDR). The common papulosis-plaque psoriasis was found to be associated with individual polymorphic variants of cytokine and CRP genes as well as with gene-gene interactions. Concerning individual polymorphic gene variants, the association strength (% entropy) with common papulosis-plaque psoriasis was as follows: TNFα_ rs361525 (16.99% entropy), IL1β_rs16944 (6.40% entropy), CRP_rs1205 (2.55% entropy), IL6_rs1554606 (1.11% entropy), IL10_rs1800896 (0.57% entropy), IL8_rs2227306 (0.30% entropy). We have found that IL6 (rs1554606) and IL8 (rs2227306) showed marked synergism, as well as moderate synergism of CRP (rs1205) and IL10 (rs1800896), and pronounced antagonism of IL1β (rs16944) and TNFα (rs361525).

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The authors declare that there are no conflicts of interest present.