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Endometriosis: the host response

C M Grosskinsky¹, J Halme

¹University of North Carolina at Chapel Hill 27599.

Bailliere'S Clinical Obstetrics and Gynaecology

|December 1, 1993

Summary

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Endometriosis may arise from immune system dysfunction, where the body fails to clear menstrual debris, leading to inflammation and scarring. Research explores immune tolerance and cell adhesion molecules in disease development.

Area of Science:

Immunology
Reproductive Medicine
Cell Biology

Background:

Abundant evidence links altered immune function to endometriosis.
Most women experience retrograde menstruation, yet only some develop endometriosis.

Purpose of the Study:

To synthesize current data on immune responses in endometriosis.
To propose conceptual frameworks explaining endometriosis pathogenesis.
To identify key areas for future research, including immune tolerance and cell adhesion molecules.

Main Methods:

Review and synthesis of existing research on immune function in endometriosis.
Exploration of hypotheses regarding uterine privilege and immune tolerance.
Investigation into the role of cell adhesion molecules (e.g., integrins).

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Main Results:

Eutopic endometrium is typically immune-privileged.
Retrograde menstruation may trigger an immune attack on ectopic endometrial tissue.
Altered immune responses, such as antibody production or breakdown of tolerance, may permit endometriosis persistence.
Differences in cell adhesion molecule behavior between eutopic and ectopic endometrium are observed.

Conclusions:

Endometriosis pathogenesis may involve a failure of normal immune tolerance to endometrial antigens.
Immune dysregulation, potentially involving antibody-mediated masking or loss of suppressor mechanisms, plays a critical role.
Cell adhesion molecules represent a promising area for future endometriosis research.