References

mimmun

Медицинская иммунология

Medical Immunology (Russia)

1563-06252313-741X

SPb RAACI

10.15789/1563-0625-2014-2-127-138

mimmun-678

Research Article

ОБЗОРЫ

REVIEWS

ИММУНОПАТОГЕНЕЗ ПСОРИАЗА И ПСОРИАТИЧЕСКОГО АРТРИТА

IMMUNE PATHOGENESIS OF PSORIASIS AND PSORIATIC ARTHRITIS

Смирнова

С. В.

Smirnova

S. V.

профессор, заместитель директора по научной работе, руководитель отдела клинической иммунологии и клеточных технологий ФГБУ «Научно-исследовательский институт медицинских проблем Севера» СО РАМН

PhD, MD (Medicine), Professor, Deputy Director for Research, The head of the Division of Clinical Immunology and Cell Technologies, Research Institute for Medical Problems of the North, Siberian Branch of Russian Academy of Medical Sciences

Смольникова

М. В.

Smolnikova

M. V.

к.б.н., ведущий научный сотрудник, лаборатория клеточно-молекулярной физиологии и патологии ФГБУ «Научно-исследовательский институт медицинских проблем Севера» СО РАМН

PhD (Biology), Leading Research Associate, Laboratory of cellular molecular physiology and pathology, Research Institute for Medical Problems of the North, Siberian Branch of Russian Academy of Medical Sciences

smarinv@ya.ru

ФГБУ «Научно-исследовательский институт медицинских проблем Севера» СО РАМН, г. КрасноярскРоссияResearch Institute for Medical Problems of the North, Siberian Branch of Russian Academy of Medical Sciences, KrasnoyarskRussian Federation

2014

01082014

162127138

2014

Смирнова С.В., Смольникова М.В.

Smirnova S.V., Smolnikova M.V.

Данная работа распространяется под лицензией Creative Commons Attribution 4.0.

This work is licensed under a Creative Commons Attribution 4.0 License.

https://www.mimmun.ru/mimmun/article/view/678

Актуальность изучения псориаза (ПС) обусловлена ростом заболеваемости, учащением случаев тяжелых форм, таких как псориатический артрит (ПсА). Клиника и исход псориаза и псориатического артрита во многом зависят от степени иммунологических нарушений и дисбаланса цитокиновой регуляции межклеточных взаимодействий. В иммунопатогенезе ПС и ПсА ведущими являются иммунные нарушения, характеризующиеся девиацией цитокинового профиля по Th1-типу (TNFα, IL-2, IFNγ и др.). Проведен анализ данных литературы, раскрывающих особенности иммунопатогенеза ПС и ПсА в ассоциации с характером течения патологического процесса. Привлечено внимание к относительно новым и малоизученным данным о роли цитокинов, продуцируемых Th17- и Th22-клетками (IL-17, IL-22, IL-23, IL-26), подсемейства цитокинов IL-19 (IL-19, IL-20 и IL-24) в патогенезе ПС и ПсА. Поиск иммунологических маркеров риска развития ПС и ПсА является важным шагом персонализированного подхода к прогнозу их течения и формированию профилактических мероприятий с целью предупреждения прогрессирования патологии.

Significance of psoriasis (PS) research is determined by increasing incidence of this disorder, higher frequency of severe clinical forms, e.g., psoriatic arthritis (PsA). Clinical course and outcomes of psoriasis and psoriatic arthritis depend on degree of immunological disturbances and imbalance of cytokine regulation of intercellular interactions. The leading immune disorders involved in pathogenesis of psoriasis and PsA are those characterized by alterations of Th1-type cytokine profile (TNFα, IL-2, IFNγ, etc.). We have analyzed publications that reveal some features of PS and PsA immunopathogenesis associated with nature of the diseases. The review draws attention to relatively new and scarcely studied data concerning the role of cytokines produced by Th17- and Th22-cells (IL-17, IL-22, IL-23, IL-26), IL-19 subfamily (IL-19, IL-20, IL-24) in development of psoriasis and PsA. Search for the immunological markers predisposing for risk of psoriasis and PsA is an important step in personalized approach to their prediction and planning of preventive measures, in order to prevent progression of this pathology.

псориазпсориатический артритцитокиныиммунопатогенез

psoriasispsoriatic arthritiscytokinesimmunopathogenesis

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