The role of cell-mediated immunity in pathogenesis of endometriosis.
It is well recognized that cell-mediated immune responses contribute to the elimination of foreign antigens and cells from the invading organism. It is also likely that the immune system can recognize and eliminate altered or misplaced autologous cells such as ectopic endometrial cells. This mechanism may be operative in most women, preventing the development of endometriosis. Recent studies in women with endometriosis demonstrate functional changes in cells of the immune system including monocytes/macrophages, natural killer cells, cytotoxic T-lymphocytes and B cells. These changes suggest decreased surveillance, recognition and destruction of the misplaced endometrial cells and possible facilitation of their implantation and development of endometriosis. Peripheral blood monocytes (PBM) and peritoneal macrophages (PM) may play a key role in this respect, and may control the function of other immune cells. We have demonstrated that in normal fertile women without endometriosis, PBM and PM suppress endometrial cell proliferation in vitro. In endometriosis, PBM stimulate and PM inhibit endometrial cell proliferation and the cytotoxic effect of PM is inversely correlated with the stage of the disease. The decrease in PM cytotoxic function is controlled by prostaglandin synthesis. In infertile women without endometriosis, the effects of PM and PBM are variable. In about one third of patients, the effects of PM and PBM suggest subclinical endometriosis; in the remaining two thirds of patients the effects of PM and PBM are similar to those of fertile controls. Interestingly, endometrial cells in women with endometriosis are more sensitive to the stimulatory effect of PBM, and more resistant to the cytotoxicity of the immune cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Dmowski
W P
WP
Institute for the Study and Treatment of Endometriosis, Chicago, Illinois.
Gebel
H M
HM
Braun
D P
DP
D001323:Autoantibodies / Q000502:physiology; D004715:Endometriosis / Q000276:immunology*; D004717:Endometrium / Q000166:cytology / Q000276:immunology; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007247:Infertility, Female / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000502:physiology; D008264:Macrophages / Q000502:physiology
D001323:Autoantibodies