子宫内膜异位症与异位局灶性炎症和免疫抑制微环境密切相关。先天免疫系统中存在多种类型的模式识别受体(PRR),它们能够在细胞内和外部环境中检测病原体相关分子模式(PAMPs)和危险相关分子模式(DAMPs)。然而,PRR在子宫内膜异位症中的确切作用和潜在的分子机制尚不清楚.PRR对于先天免疫系统识别和破坏侵入性外来感染因子是必需的。哺乳动物主要有两种类型的微生物识别系统。第一个由膜结合受体组成,如Toll样受体(TLRs),它们识别细胞外微生物并激活细胞内信号以刺激免疫反应。第二个由细胞内PRR组成,包括节点样受体(NLR)和抗病毒蛋白视黄酸诱导基因I(RIG-I)和具有螺旋酶结构域的黑色素瘤分化相关基因5(MDA-5)。在这次审查中,我们主要关注PRRs在子宫内膜异位症相关病理过程中的关键作用。PRRs识别PAMPs并能区分病原微生物和自身,触发受体配体反应,然后刺激宿主免疫反应。激活的免疫应答促进微生物感染信号向细胞的传递。由于子宫内膜异位症的特征是炎症和免疫反应失调,PRR可能与子宫内膜异位症相关炎症和免疫疾病的激活有关。Toll样受体2(TLR2),toll样受体3(TLR3),toll样受体4(TLR4),节点样受体家族胱天蛋白酶激活和募集域(CARD)含有5(NLRC5),节点样受体家族pyrin结构域含3(NLRP3),和c型凝集素受体(CLRs)通过调节免疫和炎症反应在子宫内膜异位症的发展中起重要作用。黑素瘤2(AIM2)样受体(ALR)和视黄酸诱导基因I样受体(RLR)中缺失可能参与子宫内膜异位症相关免疫和炎症疾病的激活。PRR,尤其是TLRs,可作为减轻子宫内膜异位症患者疼痛的潜在治疗靶点。PRR及其配体与先天免疫系统相互作用以增强子宫内膜异位症期间基质细胞的炎症。因此,靶向PRR及其新的合成配体可能为治疗子宫内膜异位症提供新的治疗选择.
Endometriosis is closely associated with ectopic focal inflammation and immunosuppressive microenvironment. Multiple types of pattern recognition receptors (PRRs) are present in the innate immune system, which are able to detect pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) in both intracellular and external environments. However, the exact role of PRRs in endometriosis and the underlying molecular mechanism are unclear. PRRs are necessary for the innate immune system to identify and destroy invasive foreign infectious agents. Mammals mainly have two types of microbial recognition systems. The first one consists of the membrane-bound receptors, such as toll-like receptors (
TLRs), which recognize extracellular microorganisms and activate intracellular signals to stimulate immune responses. The second one consists of the intracellular PRRs, including nod-like receptors (NLRs) and antiviral proteins retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA-5) with helix enzyme domain. In this
review, we mainly focus on the key role of PRRs in the pathological processes associated with endometriosis. PRRs recognize PAMPs and can distinguish pathogenic microorganisms from self, triggering receptor ligand reaction followed by the stimulation of host immune response. Activated immune response promotes the transmission of microbial infection signals to the cells. As endometriosis is characterized by dysregulated inflammation and immune response, PRRs may potentially be involved in the activation of endometriosis-associated inflammation and immune disorders. Toll-like receptor 2 (TLR2), toll-like receptor 3 (TLR3), toll-like receptor 4 (TLR4), nod-like receptor family caspase activation and recruitment domain (CARD) domain containing 5 (NLRC5), nod-like receptor family pyrin domain containing 3 (NLRP3), and c-type lectin receptors (CLRs) play essential roles in endometriosis development by regulating immune and inflammatory responses. Absent in melanoma 2 (AIM2)-like receptors (ALRs) and retinoic acid-inducible gene I-like receptors (RLRs) may be involved in the activation of endometriosis-associated immune and inflammation disorders. PRRs, especially
TLRs, may serve as potential therapeutic targets for alleviating pain in endometriosis patients. PRRs and their ligands interact with the innate immune system to enhance inflammation in the stromal cells during endometriosis. Thus, targeting PRRs and their new synthetic ligands may provide new therapeutic options for treating endometriosis.