Immunopathogenesis of endometriosis—A novel look at an old problem
Open accessAbstract
This review aims to cast a look at endometriosis as a chronic and progressive gynecological disease.Endometriosis-affected tissues show a variety of pathologic features: alterations in cell growth, apoptosis, activation, angiogenesis, cell adhesion, and cytokine production. Fresh endometriotic lesions are associated with induction of an inflammatory reaction represented by overproduction of prostaglandins (PGE2), metalloproteinases (MMP-2, -3, -9), cytokines (IL-1, IL-8, IFN-, TNF-, MCP-1 and MIF) and adhesive molecules (ICAM-1, VCAM-1) and activation of synthesis of reactive oxygen and nitrogen species. The inflammatory process may lead to defective folliculogenesis by an altered follicular milieu. An increase in the number and change in function of macrophages, T- and B-lymphocytes and reduction of NK cells have been reported. Treg lymphocytes are known to play an extremely important role in controlling and modulating changes in the aberrant immune response in endometriosis. Dysregulation of the immune system results in both increased progression of endometriosis and its severity. In inflammatory conditions the immune cells provide immune defense at the local level – in peritoneal fluid – and could further cause: 1) a decrease of the number of NK CD16+ cells with expression of KIRs and an increase of NK CD57+; 2) increased numbers of CD8+ cells and CD11b– immature dendritic cells; 3) an increase of FoxP3 expression in the regulatory T cell (Treg) population; 4) an increase of macrophages activating T- and B-lymphocytes leading to elevated synthesis of cytokines and/or autoantibodies. We may conclude that endometriosis resembles an immunodependent disease with the autoimmune background and breakdown of immunosuppressive mechanisms. Further immunological investigations may open a new avenue to discover innovative immunomodulatory treatments of endometriosis.
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Immunological disturbances present in endometriosis may exacerbate inflammatory processes within blood vessels, increasing the risk of developing atherosclerosis.
“Moreover, immunological disturbances present in endometriosis may exacerbate inflammatory processes within blood vessels, increasing the risk of developing atherosclerosis [6,7].”
From Endometriosis and Cardiovascular Disease: Exploring Pathophysiological Interconnections and Risk Mechanisms (2025) · cites this paper as [7]
The Immune factors and Endometriosis and autoimmunity sections describe immune disturbances and inflammation in endometriosis. The Etiology and pathogenesis section reports increased cardiovascular comorbidity but says it is unknown whether that is a consequence of endometriosis. Our copy does not connect these disturbances to inflammation within blood vessels or specifically to atherosclerosis. (LLM, conf=0.86)
Experimental — accuracy not yet measuredInflammatory processes associated with endometriosis lead to elevated levels of pro-inflammatory cytokines, such as IL-6 and TNF-α, as well as increased oxidative stress.
“Inflammatory processes associated with endometriosis lead to elevated levels of pro-inflammatory cytokines, such as IL-6 and TNF-α, as well as increased oxidative stress.”
From Endometriosis and Cardiovascular Disease: Exploring Pathophysiological Interconnections and Risk Mechanisms (2025) · cites this paper as [7]
These same mediators play a pivotal role in the pathogenesis of atherosclerosis, contributing to endothelial dysfunction and the formation of atherosclerotic plaques.
“These same mediators play a pivotal role in the pathogenesis of atherosclerosis, contributing to endothelial dysfunction and the formation of atherosclerotic plaques.”
From Endometriosis and Cardiovascular Disease: Exploring Pathophysiological Interconnections and Risk Mechanisms (2025) · cites this paper as [7]
The Humoral factors of innate immunity section identifies inflammatory mediators involved in endometriosis, but does not address their role in atherosclerosis. Searches for atherosclerosis, endothelial dysfunction, and plaque formation found no passage supporting the attributed claim. Page numbers were not available in our copy. (LLM, conf=0.76)
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- Authors
- Chopyak, V. V., Koval, H. D., Havrylyuk, A. M., Lishchuk-Yakymovych, K. A., Potomkina, H. A., & Kurpisz, M. K.
- Affiliations
- Danylo Halytsky Lviv National Medical University (UA)
- Institute of Human Genetics (PL)
- Corresponding author
- Kurpisz, Maciej K.
- Venue
- Central European Journal of Immunology
- Publisher
- Termedia Sp. z.o.o.
- Published
- 2022-03-06
- Volume
- 47
- Issue
- 1
- Pages
- 109-116
- ISSN
- 1426-3912 (ISSN-L)
- 1644-4124
- PMC
- PMC9115599
- OpenAlex
- W4225938763
- Cited by
- 41
- References
- 31
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 11 · 2023: 10 · 2022: 3
- FWCI
- 1.33
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Central European Journal of Immunology (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Narodowym Centrum Nauki (2017/25/B/NZ5/01131)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Ectopic Pregnancy Diagnosis and Management
- Keywords
- endometriosis, immunopathogenesis, chronic inflammation, prostaglandins, matrix metalloproteinases, cytokines, adhesion molecules, reactive oxygen and nitrogen species, folliculogenesis, macrophages, natural killer cells, regulatory T cells, dendritic cells, autoimmunity, immunomodulatory therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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