Objective: To provide a review of the humoral and cellular immunology of en
dometriosis and to discuss the rationale for future approaches to diagnosis
and treatment.
Design: Literature survey.
Result(s): Defective immunosurveillance in women who are destined to develo
p endometriosis may allow for the survival of ectopic endometrial tissue. T
he evidence includes endometrial cell resistance to apoptosis, perhaps thro
ugh the secretion of proteins that interfere with implant recognition and/o
r FasL expression by stromal cells, inducing apoptosis of Fas-bearing immun
e cells. Although the immune response may be defective, aspects of it clear
ly are enhanced in endometriosis, as is seen by the generalized polyclonal
B-cell autoimmune activation and secretion of immune proteins. Several cyto
kines, chemokines, and growth factors (including vascular growth factors) a
re increased in women with endometriosis.
Conclusion(s): A complex network of locally produced cytokines modulate the
growth and inflammatory behavior of ectopic endometrial implants. Proinfla
mmatory proteins from endometriotic lesions-and associated immune cells con
tribute to the enhanced inflammatory reaction associated with endometriosis
that subserves the survival of these lesions instead of leading to their d
emise. (C) 2001 by American Society for Reproductive Medicine.