The immune system probably plays a role in the onset and development of endometriosis. A general picture can be proposed. In some women refluxing endometrial cells are not destroyed, either because the patient is genetically programmed not to respond to endometrial antigens, or because the reflux is so abundant that the scavenging capacity of the peritoneal immune cells is overloaded. Refluxing cells could be protected 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 P. Immunosuppressive factors block the cytotoxic activity of natural killer (NK) cells. Activated macrophages present antigens of endometrial cells to T cells which will co-operate with B cells to synthesize autoantibodies. Synthesized antibodies protect the ectopic endometrium and could worsen the dysfunction of local NK cells. A vicious circle is set up involving all the partners of the immune system. It is as yet impossible to pinpoint the triggering mechanism. The primary defect could be localized on the endometrium, macrophages already activated by an extrinsic factor (infection, spermatozoa, chemical substances), the uterus or the tubo-uterine junction. The two pathophysiological theories put forward to explain endometriosis are linked by a defective immune system. Indeed, once the vicious circle is set up, growth and angiogenic factors could induce metaplasia of the already irritated mesothelium.

中文翻译：

---

子宫内膜异位症的免疫学方面。

免疫系统可能在子宫内膜异位症的发生和发展中起作用。可以提出一个总体情况。在某些女性中，回流的子宫内膜细胞并未被破坏，这是因为患者在基因上编程为对子宫内膜抗原无反应，或者因为回流非常丰富，以致腹膜免疫细胞的清除能力超负荷。回流细胞可以由于异常表达某些粘附分子的间皮粘附而受到保护。这些子宫内膜细胞在不被破坏的情况下会激活巨噬细胞而引起炎症。腹膜不仅保护这些子宫内膜细胞，而且还会产生异常量的趋化性和血管生成性细胞因子（白介素8）。巨噬细胞通过生长因子（例如转化生长因子P）促进发育。免疫抑制因子阻断自然杀伤（NK）细胞的细胞毒活性。活化的巨噬细胞将子宫内膜细胞的抗原呈递给T细胞，后者将与B细胞协同合成自身抗体。合成的抗体可保护异位子宫内膜，并可能加剧局部NK细胞的功能障碍。建立了一个涉及免疫系统所有伙伴的恶性循环。查明触发机制尚不可能。主要缺陷可能位于子宫内膜，已经被外在因素（感染，精子，化学物质），子宫或肾小管-子宫交界处激活的巨噬细胞上。提出用于解释子宫内膜异位症的两种病理生理学理论与免疫系统缺陷有关。确实，一旦形成恶性循环，生长和血管生成因子就可能诱发已经刺激的间皮的化生。