arthyperАртериальная гипертензия"Arterial’naya Gipertenziya" ("Arterial Hypertension")1607-419X2411-8524Antihypertensive League10.18705/1607-419X-2006-12-1-32-36arthyper-1042Research ArticleОРИГИНАЛЬНЫЕ СТАТЬИORIGINAL ARTICLESСовременные представления о роли иммунной системы в развитии гестозаModern conception about immune system role in the gestosis developmentТапильскаяН. И.TapilskayaN. ..noemail@neicon.ruСанкт-Петербургская Государственная педиатрическая медицинская академияRussian Federation2006280220061213236Copyright © Тапильская Н.И., 20062006Тапильская Н.И.Tapilskaya N...Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://htn.almazovcentre.ru/jour/article/view/1042

С иммунологических позиции преэклампсия рассматривается как результат дезадаптации иммунной системы матери, и следствие нарушения процессов плацентации, что является первым шагом в развитии заболевания. На роль кандидатов, выступающих в роли медиаторов вызывающих иммуниологическую дисфункцию претендуют провоспалительные цитокины, в частности, фактор некроза опухолей, иитерлейкин-2, интерлейкин-6. Низкий уровень HLA-G на профобласте у пациенток с преэклампсией изменяет цитокиновый профиль в сторону усиления продукции Th1 цитокинов. Отмечено частое сочетание совместимости матери и плода по антигенам HLA и гестоза в форме преэклампсии. Генетическая близость по локусу D системы HLA затрудняет распознавание аллоантигенов плода и продукцию блокирующих антител, что препятствует формированию толерантности и нарушает барьерную функцию плаценты. Цель обзора суммировать данные о патогенезе преэклампсии с точки зрения дезадаптации иммунной системы.

All at the clinical manifestations ol preeclampsia could be attributed to the endothelial cell dysfunction leading to end-organ damage and hypoperfusion. Preeclampsia is a result immune maladaptation. The candidates mediators of immune maladaptation in preeclampsia include cytokines (especially tumor necrosis factor, (TNF-a) and interleukin-2 and IL-6). In addition a lower level of messenger RNA for HLA-G has been described in the trophoblast cells of preeclamptic patients. Increased syncitiotrophoblast shedding as a consequence of placental apoptosis may contribute to endothelial dysfunction. The aim of this review is to summarize the current understanding of the pathogenesis of preeclampsia with special emphasis on recent discoveries which support the notion that immune maladaptation plays an important role in the pathogenesis of preeclampsia.

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