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Korotkova T.D.

National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of Ministry of Healthcare of Russia, Moscow, Russia

Adamyan L.V.

Department of Reproductive Medicine and Surgery, Faculty of Postgraduate Professional Education, A.I. Evdokimov Moscow State University of Medicine and Dentistry, Ministry of Health of Russia, Moscow, Russia

Stepanian A.A.

Kafedpa peppoduktivnoĭ meditsiny i xipupgii Mockovckogo univepciteta meditsiny i ctomatologii

Krechetova L.V.

National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of Ministry of Healthcare of Russia, Moscow, Russia

Vanko L.V.

National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of Ministry of Healthcare of Russia, Moscow, Russia

Cellular and molecular factors of innate immunity in the pathogenesis of external genital endometriosis in women (a review)

Authors:

Korotkova T.D., Adamyan L.V., Stepanian A.A., Krechetova L.V., Vanko L.V.

More about the authors

Journal: Russian Journal of Human Reproduction. 2018;24(6): 22‑31

DOI: 10.17116/repro20182406122

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Table of contents

CELLULAR AND MOLECULAR FACTORS OF INNATE IMMUNITY IN THE PATHOGENESIS OF EXTERNAL GENITAL ENDOMETRIOSIS IN WOMEN (A REVIEW)
CELLULAR AND MOLECULAR FACTORS OF INNATE IMMUNITY IN THE PATHOGENESIS OF EXTERNAL GENITAL ENDOMETRIOSIS IN WOMEN (A REVIEW)

To cite this article:

Korotkova TD, Adamyan LV, Stepanian AA, Krechetova LV, Vanko LV. Cellular and molecular factors of innate immunity in the pathogenesis of external genital endometriosis in women (a review). Russian Journal of Human Reproduction. 2018;24(6):22‑31. (In Russ., In Engl.)
https://doi.org/10.17116/repro20182406122

Подписка 2026 Проблемы репродукции (Russian Journal of Human Reproduction)
МСФ на ЯМ
Использование инфографики авторами научных работ
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Abstract:

ABSTRACT Literature data analysis of the role of cellular and humoral factors of inborn immunity in the pathogenesis of endometriosis is presented. Review includes the data from foreign and domestic articles for a research topic, published in the Pubmed database journals over the past 15 years. The data about contribution of cellular and humoral factors of inborn immunity acting at the local and systemic level to the pathogenesis of endometriosis are presented. Given the polyfunctionality of cells and cytokines which are the pleiotropic proteins with significant redundancy of functions, it is still difficult to determine how they affect the pathogenesis of endometriosis. The factors of inborn immunity are the significant ones in the development of endometrioid lesions. The presented data expand the knowledge of pathogenesis of endometriosis and indicate to the need for further study of the role of these factors. A deeper understanding of their mechanisms can help to improve the management of the women with external genital endometriosis and the possibility of targeted therapy application, including the influence to the factors of inborn immunity.

Keywords:

endometriosis
pathogenesis
immune dysfunction
factors of inborn immunity

Authors:

Korotkova T.D.

National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of Ministry of Healthcare of Russia, Moscow, Russia

Adamyan L.V.

Department of Reproductive Medicine and Surgery, Faculty of Postgraduate Professional Education, A.I. Evdokimov Moscow State University of Medicine and Dentistry, Ministry of Health of Russia, Moscow, Russia

Stepanian A.A.

Kafedpa peppoduktivnoĭ meditsiny i xipupgii Mockovckogo univepciteta meditsiny i ctomatologii

Krechetova L.V.

National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of Ministry of Healthcare of Russia, Moscow, Russia

Vanko L.V.

National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of Ministry of Healthcare of Russia, Moscow, Russia

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