mimmunМедицинская иммунологияMedical Immunology (Russia)1563-06252313-741XSPb RAACI10.15789/1563-0625-2013-3-203-214mimmun-625Research ArticleОБЗОРЫREVIEWSХРОНИЧЕСКАЯ КРАПИВНИЦА В ДЕТСКОМ ВОЗРАСТЕ. ИММУНОПАТОЛОГИЯ ХРОНИЧЕСКОЙ КРАПИВНИЦЫ У ДЕТЕЙ (ЧАСТЬ I)CHRONIC URTICARIAL IN CHILDHOOD. IMMUNE PATHOLOGY OF CHRONIC URTICARIAL IN CHILDREN (PART I)СинельниковаН. А.SinelnikovaN. A.

заочный аспирант кафедры факультетской педиатрии

198097, Санкт-Петербург, пр. Стачек, 32, кв. 42. Тел.: 8 (921) 302-28-00. Факс: 8 (812) 542-80-14

PhD candidate, Department of Faculty Pediatrics

198097, Stachek pr., 32, apt 42. Phone: 7 (921) 302-28-00. Fax: 7 (812) 542-80-14

N_Sinelnikova@mail.ruКалининаН. М.KalininaN. M.

д.м.н., профессор

PhD, MD (Medicine), Professor

N_Sinelnikova@mail.ruСавенковаН. Д.SavenkovaN. D.

д.м.н., профессор, кафедра факультетской педиатрии

PhD, MD (Medicine), Professor, Department of Faculty Pediatrics

N_Sinelnikova@mail.ruСанкт-Петербургский государственный педиатрический медицинский университет, Санкт- ПетербургРоссияSt. Petersburg State Pediatric Medical University, St. PetersburgRussian FederationВсероссийский центр экстренной и радиационной медицины МЧС России, Санкт-ПетербургРоссияAll-Russian Center of Extremal and Radiation Medicine, Russian Ministry of Extreme Situations, St. PetersburgRussian Federation201324072014153203214Copyright © Синельникова Н.А., Калинина Н.М., Савенкова Н.Д., 20142014Синельникова Н.А., Калинина Н.М., Савенкова Н.Д.Sinelnikova N.A., Kalinina N.M., Savenkova N.D.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/625

Резюме. В данной части обзора рассмотрены распространенность, генетические факторы предрасположенности и некоторые иммунологические механизмы хронической крапивницы у детей. Показано, что тучным клеткам и базофилам принадлежит центральная роль в патогенезе всех форм. В ходе воспалительных реакций при хроническом течении крапивницы происходит стимуляция продукции таких цитокинов, как CCL2, CХCL8, IL-1, IL-4, IL-6, IL-10, IL-13, IL-17. Активация тучных клеток и базофилов реализуется через специфические рецепторы на мембране клеток. Особое место занимает аутоиммунная крапивница, в патогенезе которой участвуют анти-FCεRIα антитела или аутоантитела к IgE, оказывающие гистамино-высвобождающее действие за счет перекрестного связывания α-цепей высокоаффинного IgE рецептора или перекрестного связывания фиксированных на тучных клетках IgE. Дегрануляция базофилов сопровождается появлением активационных молекул – СD203с, CD63. Экспрессию СD203с ряд авторов считает косвенным признаком аутоиммунного процесса, при наличии положительного теста с аутосывороткой. Повышение экспрессии лиганда CD40L на поверхности активированных Т-лимфоцитов свидетельствует об усилении сигналов для активации В-лимфоцитов и синтеза аутоантител.

Abstract. This section of our review article deals with prevalence, genetic factors, and some immune mechanisms of chronic urticaria in children. In any form of chronic urticaria, the main pathogenetic role is ascribed to mast cells and basophiles. Increased production of cyto- and chemokines, e.g., CCL2, CХCL8, IL-1, IL-4, IL-6, IL-10, IL-13, IL-17, is observed during chronic inflammatory reactions typical to this disease. Activation of mast cells and basophiles proceeds via specific receptors on the target cell membranes. Autoimmune urticaria is of special importance. In this disorder, autoantibodies are directed against IgE or FCεRIα, thus causing histamine release, due to cross-linking of α-chains of high-affinity IgE receptor, or binding of IgE fixed on the mast cells. Degranulation of basophils is followed by occurrence of activation molecules (СD203с, CD63). Some workers presumet that association between СD203с expression and positive autologous serum skin test may be a sign of autoimmune process. Increased expression of CD40L ligand on the surface of activated T cells suggests enhanced signaling for B cell activation and production of autoantibodies.

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