Role of apoptosis disturbances in external genital endometriosis

In: Russian Journal of Immunology · 2021 · vol. 24(3) , pp. 409–412 · doi:10.46235/1028-7221-1038-roa · W4285416764
article OA: diamond CC0
AI-generated summary by claude@2026-08, 2026-08-03

External genital endometriosis is associated with an imbalance in immunocompetent cell apoptosis, potentially promoting implant growth by decreasing T-lymphocyte and NK-cell cytotoxicity via the Fas-FasL pathway.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

External genital endometriosis (EGE) is currently considered one of the most common disorders in women at their reproductive age. EGE is a chronic disease that affects about 10% of women of reproductive age, leading to functional and structural changes in reproductive system, infertility, pelvic pain, and affects their quality of life. Moreover, the patients with endometriosis often suffer from depression, especially, due to pain syndrome. Endometriosis is associated with dysregulation of T-cell immune response, which presents as altered interactions between T-cells, macrophages, NK (natural killer cells), B-cells, thus allowing ectopic implantation of endometrial cells. The pronounced negative effect of EGE on the quality of life of patients, their reproductive function, impaired adaptation of the patients in community, and growing costs of treatment determine social significance of the disease and importance of appropriate studies. It is obvious that disorders of the immune system play a significant role in IGE development. However, despite extensive research in this area, the processes of apoptosis in IGE have not been sufficiently studied. Therefore, the aim of our study was to assess the origin of apoptosis disorders in women with stage I-II and III-IV of external genital endometriosis. We examined 71 patients with EGE which were divided into 2 groups: group 1 included the patients with EGE stage I-II (n = 31), and group 2, the patients with stage III-IV EGE (n = 40). The control group included 24 patients without EGE. The population profile of peripheral blood lymphocytes was determined by laser flow cytometry using Immunotex reagents, i.e., FITC-labeled CD8+, CD16+, and PE-labeled CD95+ antibodies. The number of lymphocytes entering apoptosis was detected using a diagnostic kit for AnnexinV+ (FITC) and PI+ from Caltag. The results were read on a BECKMAN COULTER EPICS XL-II flow cytometer using standard protocols.An imbalance between activation and apoptosis of immunocompetent cells may be a significant cause of EGE. Induction of apoptosis by the Fas-FasL pathway in patients with external genital endometriosis leads to decreased cytotoxicity mediated by T-lymphocytes and NK-cells. A statistically significant decrease in the content of AnnexinV+ presenting lymphocytes suggests impairment of their receptor-dependent apoptosis.Altered apoptosis processes may be responsible for the development of IGE by promotion of proliferation and growth of endometrioid implants.
Full text 4,995 characters · extracted from oa-html · 3 sections · click to expand

Abstract

External genital endometriosis (EGE) is currently considered one of the most common disorders in women at their reproductive age. EGE is a chronic disease that affects about 10% of women of reproductive age, leading to functional and structural changes in reproductive system, infertility, pelvic pain, and affects their quality of life. Moreover, the patients with endometriosis often suffer from depression, especially, due to pain syndrome. Endometriosis is associated with dysregulation of T-cell immune response, which presents as altered interactions between T-cells, macrophages, NK (natural killer cells), B-cells, thus allowing ectopic implantation of endometrial cells. The pronounced negative effect of EGE on the quality of life of patients, their reproductive function, impaired adaptation of the patients in community, and growing costs of treatment determine social significance of the disease and importance of appropriate studies. It is obvious that disorders of the immune system play a significant role in IGE development. However, despite extensive research in this area, the processes of apoptosis in IGE have not been sufficiently studied. Therefore, the aim of our study was to assess the origin of apoptosis disorders in women with stage I-II and III-IV of external genital endometriosis. We examined 71 patients with EGE which were divided into 2 groups: group 1 included the patients with EGE stage I-II (n = 31), and group 2, the patients with stage III-IV EGE (n = 40). The control group included 24 patients without EGE. The population profile of peripheral blood lymphocytes was determined by laser flow cytometry using Immunotex reagents, i.e., FITC-labeled CD8+, CD16+, and PE-labeled CD95+ antibodies. The number of lymphocytes entering apoptosis was detected using a diagnostic kit for AnnexinV+ (FITC) and PI+ from Caltag. The results were read on a BECKMAN COULTER EPICS XL-II flow cytometer using standard protocols. An imbalance between activation and apoptosis of immunocompetent cells may be a significant cause of EGE. Induction of apoptosis by the Fas-FasL pathway in patients with external genital endometriosis leads to decreased cytotoxicity mediated by T-lymphocytes and NK-cells. A statistically significant decrease in the content of AnnexinV+ presenting lymphocytes suggests impairment of their receptor-dependent apoptosis. Altered apoptosis processes may be responsible for the development of IGE by promotion of proliferation and growth of endometrioid implants.

Keywords

About the authors T. G. Avanesova Private Clinical Hospital of Russian Railways-Medicine Author for correspondence. Email: [email protected] Avanesova Tatevik G. - PhD (Medicine), Obstetrician-gynecologist 344011, Rostov-on-Don, Varfolomeev str., 92a Russian FederationM. A. Levkovich Rostov State Medical University PhD, MD (Medicine), Associate Professor, Leading Research Associate, Department of Allergic and Autoimmune Diseases Rostov-on-Don N. V. Ermolova Rostov State Medical University PhD, MD (Medicine), Head, Obstetric and Gynecological Department Rostov-on-Don I. I. Krukier Rostov State Medical University PhD, MD (Biology), Leading Research Associate, Obstetric and Gynecological Department Rostov-on-Don M. V. Dudareva Rostov State Medical University PhD, MD (Biology), Head, Clinical Diagnostic Laboratory Rostov-on-Don

References

- Адамян Л.В., Фархат К.Н., Макиян З.Н., Савилова А.М. Молекулярно-биологическая характеристика эутопического эндометрия // Проблемы репродукции, 2015. Т. 21, № 5. C. 8-16. - Красильникова А.К., Малышкина А.И., Сотникова Н.Ю., Анциферова Ю.С. Клиника «малых» форм эндометриоза // Вестник Ивановской медицинской академии, 2018. Т. 23, № 3. С. 18-21. - Левкович М.А., Ермолова Н.В., Аванесова Т.Г., Маркарьян И.В. Современные взгляды на патогенез генитального эндометриоза: роль гормональных, иммунологических, генетических факторов // Таврический медико-биологический вестник, 2017. Т. 20, № 2. C. 185-189. - Сельков С.А., Ярмолинская М.И. Эндометриоз как патология регуляторных механизмов // Журнал акушерства и женских болезней, 2017. Т. 66, № 2. С. 9-13. - Ermolova N.V., Petrov Y.A., Levkovich M.A., Kolesnikova L.V., Drukker N.A. Influence of cytokines production, nitrogen oxide metabolites and lipids exchange on the formation of external genital endometriosis stages in patients of reproductive age. Periodico Tche Quimica, 2020, Vol. 17, no. 35, pp. 813-824.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-html

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosisinfertility

Citation neighborhood (sparse)

Too few in-corpus citations on either side for a chart; here are the lists.

Cites (1)

References (1)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK