Vetvicka Vaclav, Laganà Antonio Simone, Salmeri Francesca Maria, Triolo Onofrio, Palmara Vittorio Italo, Vitale Salvatore Giovanni, Sofo Vincenza, Králíčková Milena
Department of Pathology, University of Louisville, Louisville, KY, 40202, USA.
Unit of Gynecology and Obstetrics, Department of Human Pathology in Adulthood and Childhood "G. Barresi", University of Messina, Via C. Valeria 1, 98125, Messina, Italy.
Arch Gynecol Obstet. 2016 Nov;294(5):897-904. doi: 10.1007/s00404-016-4195-6. Epub 2016 Sep 15.
Endometriosis is defined as the presence of endometrial-like endometrial cells, glands and stroma outside the uterus, causing a strong inflammatory-like microenvironment in the affected tissue. This may provoke a breakdown in the peritoneal cavity homeostasis, with the consequent processes of immune alteration, documented by peripheral mononuclear cells recruitment and secretion of inflammatory cytokines in early phases and of angiogenic and fibrogenic cytokines in the late stages of the disease. Considering the pivotal role of interaction between immune and endometriotic cells, in this paper, we aim to shed light about the role of apoptosis pathways in modulating the fine-regulated peritoneal microenvironment during endometriosis.
Narrative overview, synthesizing the findings of literature retrieved from searches of computerized databases.
In normal conditions, endometriotic cells, refluxed through the fallopian tubes into the peritoneal cavity, should be attacked and removed by phagocytes and NK cells. During endometriosis, the breakdown of peritoneal homeostasis causes the failure of scavenging mechanisms, allowing the survival of endometriotic cells. The consequent so-called "immunoescaping" of endometriotic cells could be due, at least in part, to the reduction of apoptotic-mediated pathways previously described.
Considering the large amount of evidence retrieved from in vitro as well as in vivo models, the reduced apoptosis of endometriotic cells together with the increased apoptosis of peritoneal fluid mononuclear cells may address the peritoneal homeostasis to a permissive environment for the progression of the disease.
子宫内膜异位症的定义为子宫外存在类似子宫内膜的细胞、腺体和间质，在受影响的组织中引发强烈的炎症样微环境。这可能会破坏腹膜腔的稳态，随之出现免疫改变过程，早期表现为外周单核细胞募集和炎症细胞因子分泌，疾病后期则表现为血管生成和纤维生成细胞因子分泌。考虑到免疫细胞与子宫内膜异位细胞之间相互作用的关键作用，本文旨在阐明凋亡途径在调节子宫内膜异位症期间精细调控的腹膜微环境中的作用。
叙述性综述，综合从计算机数据库检索中获取的文献研究结果。
在正常情况下，通过输卵管反流至腹膜腔的子宫内膜异位细胞应被吞噬细胞和自然杀伤细胞攻击并清除。在子宫内膜异位症期间，腹膜稳态的破坏导致清除机制失效，使子宫内膜异位细胞得以存活。子宫内膜异位细胞随后出现的所谓“免疫逃逸”，至少部分可能归因于先前所述的凋亡介导途径的减少。
考虑到从体外和体内模型中获得的大量证据，子宫内膜异位细胞凋亡减少以及腹膜液单核细胞凋亡增加，可能会使腹膜稳态转变为有利于疾病进展的环境。
