Mesenchymal Stromal Cells Are More Immunosuppressive In Vitro If They Are Derived from Endometriotic Lesions than from Eutopic Endometrium

Fawaz Abomaray, Sebastian Gidlöf, Cecilia Götherström
Stem cells international · 2017 · vol. 2017 , pp. 1–13 · doi:10.1155/2017/3215962 · PMID:29230250 · W2766694229
article OA: gold CC0 ⤵ 12 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Mesenchymal stromal cells isolated from endometriotic lesions exhibit a more immunosuppressive phenotype and induce M2 macrophages compared to those from eutopic endometrium.

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Abstract

Endometriosis is an inflammatory disease with predominance of immunosuppressive M2 macrophages in the pelvic cavity that could be involved in the pathology through support and immune escape of ectopic lesions. Mesenchymal stromal cells (MSC) are found in ectopic lesions, and MSC from nonendometriosis sources are known to induce M2 macrophages. Therefore, MSC were hypothesized to play a role in the pathology of endometriosis. The aim was to characterize the functional phenotype of MSC in ectopic and eutopic endometrium from women with endometriosis. Stromal cells from endometriotic ovarian cysts (ESC cyst ) and endometrium (ESC endo ) were examined if they exhibited a MSC phenotype. Then, ESC were phenotypically examined for protein and gene expression of immunosuppressive and immunostimulatory molecules. Finally, ESC were functionally examined for their effects on monocyte differentiation into macrophages. ESC cyst and ESC endo expressed MSC markers, formed colonies, and differentiated into osteoblasts and adipocytes. Phenotypically, ESC cyst were more immunosuppressive, with significantly higher expression of immunosuppressive molecules. Functionally, ESC cyst induced more spindle-shaped macrophages, with significantly higher expression of CD14 and CD163, both features of M2 macrophages. The results suggest that ESC cyst may be more immunosuppressive than ESC endo and may promote immunosuppressive M2 macrophages that may support growth and reduce immunosurveillance of ectopic lesions.

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endometriosis

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