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

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.