D I Lebovic1, M D Mueller, R N Taylor. 1. Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, Michigan, USA.
Abstract
OBJECTIVE: To provide a review of the humoral and cellular immunology of endometriosis 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 develop endometriosis may allow for the survival of ectopic endometrial tissue. The evidence includes endometrial cell resistance to apoptosis, perhaps through the secretion of proteins that interfere with implant recognition and/or FasL expression by stromal cells, inducing apoptosis of Fas-bearing immune cells. Although the immune response may be defective, aspects of it clearly are enhanced in endometriosis, as is seen by the generalized polyclonal B-cell autoimmune activation and secretion of immune proteins. Several cytokines, chemokines, and growth factors (including vascular growth factors) are increased in women with endometriosis. CONCLUSION(S): A complex network of locally produced cytokines modulate the growth and inflammatory behavior of ectopic endometrial implants. Proinflammatory proteins from endometriotic lesions and associated immune cells contribute to the enhanced inflammatory reaction associated with endometriosis that subserves the survival of these lesions instead of leading to their demise.
OBJECTIVE: To provide a review of the humoral and cellular immunology of endometriosis 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 develop endometriosis may allow for the survival of ectopic endometrial tissue. The evidence includes endometrial cell resistance to apoptosis, perhaps through the secretion of proteins that interfere with implant recognition and/or FasL expression by stromal cells, inducing apoptosis of Fas-bearing immune cells. Although the immune response may be defective, aspects of it clearly are enhanced in endometriosis, as is seen by the generalized polyclonal B-cell autoimmune activation and secretion of immune proteins. Several cytokines, chemokines, and growth factors (including vascular growth factors) are increased in women with endometriosis. CONCLUSION(S): A complex network of locally produced cytokines modulate the growth and inflammatory behavior of ectopic endometrial implants. Proinflammatory proteins from endometriotic lesions and associated immune cells contribute to the enhanced inflammatory reaction associated with endometriosis that subserves the survival of these lesions instead of leading to their demise.
Authors: Stacey A Missmer; Jorge E Chavarro; Susan Malspeis; Elizabeth R Bertone-Johnson; Mark D Hornstein; Donna Spiegelman; Robert L Barbieri; Walter C Willett; Susan E Hankinson Journal: Hum Reprod Date: 2010-03-23 Impact factor: 6.918
Authors: Holly R Harris; Jorge E Chavarro; Susan Malspeis; Walter C Willett; Stacey A Missmer Journal: Am J Epidemiol Date: 2013-02-03 Impact factor: 4.897
Authors: Fritz Wieser; Rene Wenzl; Clemens Tempfer; Christoph Worda; Johannes Huber; Christian Schneeberger Journal: J Assist Reprod Genet Date: 2002-07 Impact factor: 3.412
Authors: Samuel A Pauli; Donna R Session; Weirong Shang; Kirk Easley; Friedrich Wieser; Robert N Taylor; Keely Pierzchalski; Joseph L Napoli; Maureen A Kane; Neil Sidell Journal: Reprod Sci Date: 2013-02-20 Impact factor: 3.060