Endometriosis and autologous lymphocyte activation by endometrial cells. Are lymphocytes or endometrial cell defects responsible?

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Endometrial cells from women with endometriosis demonstrate reduced mitogenicity towards autologous lymphocytes, suggesting a defect in the endometrial cells rather than the lymphocytes themselves.

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Abstract

OBJECTIVE: To determine whether the decreased mitogenicity of the endometrial cell for autologous lymphocytes noted in women with pelvic endometriosis is secondary to endometrial cell interaction with the lymphocytes or due to an inherent defect of the lymphocyte. STUDY DESIGN: The endometrial cells from 30 women with endometriosis and 30 matching controls were cultured. Autologous lymphocyte and endometrial cells were cocultured to observe the lymphocyte proliferative response to autologous endometrium in controls and to ectopic and eutopic endometrial cells from patients. The ability of lymphocytes to be stimulated by phytohemagglutinin (PHA) was simultaneously assayed. RESULTS: Ectopic and eutopic endometrial cells from women with endometriosis were less mitogenic for autologous lymphocytes than endometrial cells from controls. The lymphocytes from both patients and controls exhibited a similar stimulatory response to PHA. CONCLUSION: The diminished proliferative response of lymphocytes from women with endometriosis probably is not the consequence of an intrinsic lymphocyte abnormality. The fundamental defect in endometriosis may reside within the endometrial cell.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Lymphocyte Activation Lymphocyte Activation Lymphocytes Adult Adult Cells, Cultured Cells, Cultured Coculture Techniques Coculture Techniques Endometriosis Endometriosis Female Female Humans Humans Lymphocytes Lymphocytes Phytohemagglutinins Phytohemagglutinins

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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Source provenance

europepmc
last seen: 2026-10-13T06:10:10.580696+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-08T22:00:10.289599+00:00
License: CC0 · commercial use OK