IMMUNOLOGICAL ASPECTS OF ENDOMETRIOSIS

The immune system probably plays a role in the onset and development o f endometriosis. A general picture can be proposed, In some women refl uxing endometrial cells are not destroyed, either because the patient is genetically programmed not to respond to endometrial antigens, or b ecause the reflux is so abundant that the scavenging capacity of the p eritoneal immune cells is overloaded, Refluxing cells could be protect ed due to an abnormal adherence to the mesothelium which exceptionally expresses certain adhesive molecules, Undestroyed, these endometrial cells would cause an inflammation with activation of macrophages, Not only does the peritoneum protect these endometrial cells, but it also produces abnormal quantities of chemotactic and angiogenic cytokines ( interleukin-8), Macrophages facilitate development via growth factors such as transforming growth factor beta, Immunosuppressive factors blo ck the cytotoxic activity of natural killer (NK) cells, Activated macr ophages present antigens of endometrial cells to T cells which will co -operate with B cells to synthesize autoantibodies. Synthesized antibo dies protect the ectopic endometrium and could worsen the dysfunction of local NK cells, A vicious circle is set up involving all the partne rs of the immune system, It is as yet impossible to pinpoint the trigg ering mechanism, The primary defect could be localized on the endometr ium, macrophages already activated by an extrinsic factor (infection, spermatozoa, chemical substances), the uterus or the tubo-uterine junc tion, The two pathophysiological theories put forward to explain endom etriosis are linked by a defective immune system, Indeed, once the vic ious circle is set up, growth and angiogenic factors could induce meta plasia of the already irritated mesothelium.