Immunobiology of endometriosis

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.