ssmuБюллетень сибирской медициныBulletin of Siberian Medicine1682-03631819-3684Siberian State Medical University, the Ministry of Healthcare of the Russian Federation10.20538/1682-0363-2019-3-203-213ssmu-2418Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEW AND LECTURESЭкспериментальные модели дерматологических заболеваниийExperimental models of dermatological diseaseshttps://orcid.org/0000-0003-0819-1967СергееваО. Н.SergeevaO. N.

ассистент, кафедра патологической физиологии,

660022, г. Красноярск, ул. Партизана Железняка, 1

Assistant, Department of Pathological Physiology,

1, P. Zheleznyaka Str., Krasnoyarsk, 660022

On_210@mail.ruhttps://orcid.org/0000-0001-7660-700XАксененкоМ. Б.AksenenkoM. B.

канд. мед. наук, доцент, кафедра патологической физиологии,

660022, г. Красноярск, ул. Партизана Железняка, 1

PhD, Assistant of Professor, Department of Pathological Physiology,

1, P. Zheleznyaka Str., Krasnoyarsk, 660022

https://orcid.org/0000-0001-5434-7155ФефеловаЮ. А.FefelovaYu. F.

д-р биол. наук, доцент, кафедра патологической физиологии,

660022, г. Красноярск, ул. Партизана Железняка, 1

DBSc, Assistant of Professor, Department of Pathological Physiology,

1, P. Zheleznyaka Str., Krasnoyarsk, 660022

https://orcid.org/0000-0002-2089-6022СергееваЕ. Ю.SergeevaE. Yu.

д-р биол. наук, профессор, кафедра патологической физиологии,

660022, г. Красноярск, ул. Партизана Железняка, 1

DBSc, Professor, Department of Pathological Physiology,

1, P. Zheleznyaka Str., Krasnoyarsk, 660022

https://orcid.org/0000-0001-8142-4283РукшаТ. Г.RukshaT. G.

д-р мед. наук, профессор, зав. кафедрой патологической физиологии,

660022, г. Красноярск, ул. Партизана Железняка, 1

DM, Head of Department of Pathophysiology,

1, P. Zheleznyaka Str., Krasnoyarsk, 660022

Красноярский государственный медицинский университет им. проф. В.Ф. Войно-Ясенецкого (КрасГМУ им. проф. В.Ф. Войно-Ясенецкого)РоссияKrasnoyarsk State Medical University n.a. prof. V.F. Voyno-Yasenetsky (KrasSMU n.a. prof. V.F. Voyno-Yasenetsky)Russian Federation201927102019183203213Copyright © Сергеева О.Н., Аксененко М.Б., Фефелова Ю.А., Сергеева Е.Ю., Рукша Т.Г., 20192019Сергеева О.Н., Аксененко М.Б., Фефелова Ю.А., Сергеева Е.Ю., Рукша Т.Г.Sergeeva O.N., Aksenenko M.B., Fefelova Y.F., Sergeeva E.Y., Ruksha T.G.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://bulletin.ssmu.ru/jour/article/view/2418

В статье представлен анализ экспериментальных моделей атопического дерматита, псориаза, кожных проявлений аутоиммунных системных заболеваний соединительной ткани, буллезных дерматозов. Описаны экспериментальные модели, отражающие различные стадии и типы атопического дерматита, позволяющие исследовать патогенез заболевания. Атопический дерматит может развиваться спонтанно, у мышей инбредной линии Nc/Nga существуют модели атопического дерматита, вызываемые введением аллергенов, моноклональных IgE либо при эпикутантной сенсибилизации, когда имитируется дисфункция дермального барьера. Генетически модифицированные модели атопического дерматита – трансгенные и нокаутные мыши – удобны для изучения стадийности заболевания, роли цитокинов, антигенпрезентирующих клеток и Т-лимфоцитов в патогенезе. Показано, что модели псориаза, полученные методами генной инженерии, наиболее удобны для исследования роли специфических факторов или определенного вида клеток в развитии заболевания. У трансгенных мышей происходит повышение экспрессии молекул адгезии, цитокинов, факторов транскрипции и медиаторов воспаления как в кератиноцитах, так и в клетках иммунной системы, что позволяет выявить их роль в патогенезе псориаза. Описаны варианты моделей кожных проявлений системных аутоиммунных заболеваний соединительной ткани, буллезных дерматозов с генетическими изменениями и без применения генетических модификаций. Каждая модель отражает те или иные особенности патогенеза и клинической картины, комплексное их использование позволит наиболее эффективно исследовать механизмы развития атопического дерматита, псориаза, поражений кожи при системных аутоиммунных заболеваниях соединительной ткани, буллезных дерматозах, способствуя созданию современных эффективных методов лечения. 

This review presents analysis of experimental models of atopic dermatitis, psoriasis, skin symptoms of autoimmune systemic connective tissue diseases, and blistering skin diseases. Presented in the review are experimental models of atopic dermatitis which reproduce various stages and types of disease that allows the investigation of disease pathogenesis. Atopic dermatitis can develop spontaneously in Nc/Nga mice. There are atopic dermatitis models initiated by monoclonal IgE injection or epicutant sensitization under dermal barrier disfunction imitation. Genetically modified atopic dermatitis models - transgenic and knockout mice – are convenient for investigation of disease stages, cytokines, antigen-presenting cells and T-cells influence. We show that the psoriasis models created by genetic engineering methods are the most convenient for investigation of the role of particular cell types and specific factors in the disease development. Up-regulation of adhesion molecules, cytokines, transcription factors, inflammation mediators in both keratinocytes and immune cells of transgenic mice reveals their influence on psoriasis pathogenesis. There are descriptions of skin symptom models of autoimmune systemic connective tissue diseases and blistering skin disease models with and without genetic modifications. Each model demonstrates some peculiarities of pathogenesis and disease symptoms, whereas combined use of the models will allow to study the mechanisms of development of atopic dermatitis, psoriasis, blistering skin diseases and skin lesions under autoimmune systemic connective tissue diseases, that will contribute to the development of modern effective methods of treatment.

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