References

medsovet

Медицинский Совет

Meditsinskiy sovet = Medical Council

2079-701X2658-5790

REMEDIUM GROUP Ltd.

10.21518/ms2024-057

medsovet-8240

Research Article

ИММУНОЛОГИЯ

IMMUNOLOGY

Интерферон гамма как триггер хронических вирусных инфекций и воспалительных дерматозов

Interferon gamma as a trigger of chronic viral infections and inflammatory dermatoses

https://orcid.org/0000-0003-2694-8900

Евдокимов

Е. Ю.

Evdokimov

E. Yu.

Евдокимов Евгений Юрьевич, к.м.н., врач-дерматовенеролог отделения дерматовенерологии и косметологии, Поликлиника №1 Управления делами Президента Российской Федерации; научный сотрудник клинического отдела, Центральный научно-исследовательский институт эпидемиологии

119002, Москва, пер. Сивцев Вражек, д. 26/28,

111123, Москва, ул. Новогиреевская, д. 3а

Evgenii Yu. Evdokimov, Cand. Sci. (Med.), Dermatovenerologist, Department of Dermatovenereology and Cosmetology, Polyclinic No. 1 of the Administrative Department of the Russian Federation; Researcher, Clinical Department, Central Research Institute of Epidemiology

26/28, Sivtsev Vrazhek Lane, Moscow, 119002,

3a, Novogireevskaya St., Moscow, 111123

evdokimovevg@yandex.ru

https://orcid.org/0000-0002-5885-4872

Свечникова

Е. В.

Svechnikova

E. V.

Свечникова Елена Владимировна, д.м.н., профессор кафедры кожных и венерических болезней, Российский биотехнологический университет (РОСБИОТЕХ); заведующая отделением дерматовенерологии и косметологии, Поликлиника №1 Управления делами Президента Российской Федерации

125080, Россия, Москва, Волоколамское шоссе, д. 11,

119002, Москва, пер. Сивцев Вражек, д. 26/28

Elena V. Svechnikova, Dr. Sci. (Med.), Professor of the Department of Skin and Sexually Transmitted Diseases, Russian Biotechnological University (BIOTECH University); Head of the Department of Dermatology and Cosmetology, Polyclinic No. 1 of the Administrative Department of the Russian Federation

11, Volokolamskoe Shosse, Moscow, 125080,

26/28, Sivtsev Vrazhek Lane, Moscow, 119002

elene-elene@bk.ru

https://orcid.org/0000-0002-6539-4878

Понежева

Ж. Б.

Ponezheva

Zh. B.

Понежева Жанна Бетовна, д.м.н., заведующий клиническим отделом

111123, Москва, ул. Новогиреевская, д. 3а

Zhanna B. Ponezheva, Dr. Sci. (Med.), Head of Clinical Department

3a, Novogireevskaya St., Moscow, 111123

doktorim@mail.ru

Поликлиника №1 Управления делами Президента Российской Федерации; Центральный научно-исследовательский институт эпидемиологииРоссияPolyclinic No. 1 of the Administrative Department of the Russian Federation; Central Research Institute of EpidemiologyRussian Federation

Поликлиника №1 Управления делами Президента Российской Федерации; Российский биотехнологический университет (РОСБИОТЕХ)РоссияPolyclinic No. 1 of the Administrative Department of the Russian Federation; Russian Biotechnological University (BIOTECH University)Russian Federation

Центральный научно-исследовательский институт эпидемиологииРоссияCentral Research Institute of EpidemiologyRussian Federation

2024

11052024

05214220

2024

Евдокимов Е.Ю., Свечникова Е.В., Понежева Ж.Б.

Evdokimov E.Y., Svechnikova E.V., Ponezheva Z.B.

Данная работа распространяется под лицензией Creative Commons Attribution 4.0.

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

https://www.med-sovet.pro/jour/article/view/8240

Интерферон гамма – единственный представитель семейства интерферонов 2-го типа, регулирующий Th1 и Th2 иммунный ответ. Открытие интерферона гамма связывают с именем Э. Фредерика Уилока. Экспрессия гена IFNG обеспечивает плейотропный эффект для интерферона гамма, основными иммунными направлениями данного цитокина являются противовирусный, антибактериальный и антипротозойный. В публикациях, посвященных взаимосвязи тяжести воспалительных дерматозов (псориаз, себорейный дерматит, атопический дерматит) и уровней продукции интерферона гамма, к сожалению, нет единого мнения о прямом единении этих событий. Хотя в большинстве случаев при острых вирусных заболеваниях на начальных этапах отмечается повышение продукции интерферона, при некоторых ОРВИ (COVID-19 и др.) не фиксируется его нарастание. В случаях хронических вирусных заболеваний, вызванных ретровирусными инфекциями – вирусом иммунодефицита человека, Т-лимфотропным вирусом человека типа 1 и эндогенными ретровирусами человека, в результате длительного воздействия интерферона гамма на ткани может отмечаться их повреждение, а также изменение функционального состояния CD4+ T-клеток. В случаях заболеваний, вызванных вирусом простого герпеса 2-го типа, интерферон гамма также оказывает сложное влияние на межклеточные взаимосвязи инфицированных и неинфицированных кератиноцитов, а также на процессы апоптоза у мигрирующих в дерму клеток Лангерганса, что вызывает нарушение привлечения в очаг CD4+ и CD8+ Т-лимфоцитов. При аутоиммунных заболеваниях интерферон гамма может оказывать разнонаправленное действие. В частности, у пациентов с рассеянным склерозом он регулирует процессы нейровоспаления и в зависимости от концентрации может либо снижать количество CD11b+ миелоидных клеток центральной нервной системы, уменьшать инфильтрацию воспаленных клеток и нормализовывать процессы демиелинизации, либо при повышении продукции приводить к обратным эффектам. При этом доказано усиление интерферона гамма для факторов транскрипции дифференциально экспрессируемых генов в случае развития у пациентов системной красной волчанки.

Interferon-gamma (IFN-γ) is the only representative of the type II interferon family regulating Th1 and Th2 immune responses. The discovery of IFN-γ is associated with the name of E. Frederick Wheelock. The expression of the IFNG gene provides a pleiotropic effect for IFN-γ, the main immune directions of this cytokine are antiviral, antibacterial and antiprotozoal. Unfortunately, in publications devoted to the relationship between the severity of inflammatory dermatoses (psoriasis, seborrheic dermatitis, atopic dermatitis) and levels of interferon gamma production, there is no consensus on the direct unity of these events. Although in most cases with acute viral diseases, an increase in interferon production is noted at the initial stages, but in some acute respiratory viral infections, its increase is not recorded (COVID-19, etc.), in cases of chronic viral diseases caused by retroviral infections – human immunodeficiency virus, human type 1 T-lymphotropic virus and endogenous human retroviruses as a result of prolonged exposure to IFN-γ on tissues, their damage may be noted, as well as a change in the functional state of CD4+ T cells. In cases of diseases caused by the herpes simplex virus 2, IFN-γ also has a complex effect on the intercellular relationships of infected and uninfected keratinocytes, as well as on the processes of apoptosis in Langerhans cells migrating to the dermis, which causes a violation of CD4+ and CD8+ involvement in the focus+ T-lymphocytes. In autoimmune diseases, IFN-γ can have a multidirectional effect. In particular, in patients with multiple sclerosis, IFN-γ regulates the processes of neuroinflammation and, depending on the concentration, can either reduce the number of CD11b+ myeloid cells of the central nervous system and reduce the infiltration of inflamed cells and normalize the processes of demyelination, or with an increase in IFN-γ production lead to reverse effects. At the same time, an enhancement of IFN-γ for transcription factors of differentially expressed genes in the case of systemic lupus erythematosus in patients has been proven.

интерферон гаммавоспалительные дерматозыгерпетическая инфекциявирус иммунодефицита человека

interferon gammainflammatory dermatosesherpetic infectionhuman immunodeficiency virus

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