Moghaddam Maryam Zare, Ansariniya Hossein, Seifati Seyed Mohammad, Zare Fateme, Fesahat Farzaneh
Reproductive Immunology Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Am J Reprod Immunol. 2022 May;87(5):e13537. doi: 10.1111/aji.13537. Epub 2022 Mar 15.
Endometriosis is a chronic inflammatory disease associated with the growth and proliferation of endometrial-like tissues outside the uterus. Although the exact etiology and mechanism of the pathogenesis of the disease have not been fully elucidated, the immune system cells and the mediators produced by them can be named as effective factors in the onset and progression of the disease.
We aim to attempt to review studies on the role of the immune system in endometriosis to better understand the pathogenesis of endometriosis.
Abundant production of inflammatory mediators by neutrophils and macrophages and reduced cytotoxicity of defined cells promote endometriosis at the early stages of the disease. Following an increase in the inflammation of the environment, the body takes compensatory mechanisms to reduce inflammation and establish homeostasis. For this purpose, the body produces remodeling and anti-inflammatory factors leading to slow conversion of the inflammatory environment into a non-inflammatory environment with proliferative and immunosuppressive properties. Environmental conditions induce M2 macrophages, TH2 cells, and Tregs differentiation, promoting disease progression by producing angiogenic and immunosuppressive factors. However, the exact molecular mechanism involved in changing inflammatory to non-inflammatory conditions is not yet fully understood.
Due to the common characteristics of endometriotic cells and cancer cells, most potential treatment options for endometriosis have been suggested due to the results of these methods in the treatment of cancer. In this pathway, immune system cells and soluble mediators can be used as targets.
子宫内膜异位症是一种慢性炎症性疾病，与子宫外子宫内膜样组织的生长和增殖相关。尽管该疾病的确切病因和发病机制尚未完全阐明，但免疫系统细胞及其产生的介质可被视为疾病发生和发展的有效因素。
我们旨在尝试综述关于免疫系统在子宫内膜异位症中作用的研究，以更好地理解子宫内膜异位症的发病机制。
中性粒细胞和巨噬细胞大量产生炎症介质，特定细胞的细胞毒性降低，在疾病早期促进子宫内膜异位症。随着周围炎症增加，机体采取代偿机制减轻炎症并建立内环境稳态。为此，机体产生重塑和抗炎因子，导致炎症环境缓慢转变为具有增殖和免疫抑制特性的非炎症环境。环境条件诱导M2巨噬细胞、TH2细胞和调节性T细胞分化，通过产生血管生成和免疫抑制因子促进疾病进展。然而，炎症状态转变为非炎症状态的确切分子机制尚未完全明确。
由于子宫内膜异位细胞和癌细胞具有共同特征，大多数子宫内膜异位症的潜在治疗方案是基于这些方法在癌症治疗中的结果提出的。在这一途径中，免疫系统细胞和可溶性介质可作为靶点。
