从免疫角度看子宫内膜异位症:一种基于免疫失调的病理生理学

Alison McCallion, Danielle J. Sisnett, Katherine B. Zutautas, Donya Hayati, Katherine G. Spiess, Stanimira Aleksieva, Harshavardhan Lingegowda, M. Koti, C. Tayade
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摘要

子宫内膜异位症(EMS)是一种炎症性妇科疾病,其特征是子宫外子宫内膜组织生长。由于没有令人满意的治疗方法或非侵入性诊断方法,EMS病理生理学的观点早就应该转变了。免疫失调在EMS发病机制和疾病进展中的意义一直是一个不断发展的研究领域,已经确定了许多免疫和炎症途径。关于子宫内膜异位病变建立的传统理论缺乏对其增殖和存活的机制解释,直到最近的研究发现间充质干细胞(MSC)和骨髓源性抑制细胞(MDSCs)参与了免疫内分泌信号的复杂网络。EMS独特的免疫学可能是由于雌激素的优势,因为内分泌失衡确实会导致免疫失调。EMS中观察到的许多现象与各种癌症中的免疫生物学相似,包括子宫内膜上皮细胞的体细胞突变加速。在这里,高突变负荷导致EMS新抗原的发展,这可能有助于损伤免疫微环境。此外,EMS表现出与几种慢性炎症性疾病的共病,这些疾病共有白细胞介素-23(IL-23)/IL-17通路的失调(如炎症性肠病、银屑病和类风湿性关节炎中所见)。EMS与慢性盆腔疼痛(CPP)的研究尤其相关,因为60%的EMS患者都有这种症状,而慢性炎症被认为是疼痛致敏过程的核心。由于该疾病的发病通常发生在青春期,而只有在出现中度至重度症状后几年才能进行诊断,因此创新非侵入性诊断工具以进行早期检测至关重要。一些潜在的生物标志物正在研究中,包括一些细胞因子、基因特征和细胞外小泡(EV)特征。通过将EMS的免疫观点纳入我们的研究、诊断方法和治疗解决方案,该领域有了更有希望的途径来明确定义EMS并为患者提供缓解。
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Endometriosis through an immunological lens: a pathophysiology based in immune dysregulation
Endometriosis (EMS) is an inflammatory, gynaecologic disease characterized by the growth of endometrial tissues outside the uterus. With no satisfactory therapies or non-invasive diagnostics available, a shift in perspectives on EMS pathophysiology is overdue. The implication of immune dysregulation in EMS pathogenesis and disease progression has been an evolving area of research, with numerous immune and inflammatory pathways identified. Traditional theories regarding the establishment of endometriotic lesions have lacked mechanistic explanations for their proliferation and survival until recent research unearthed the involvement of mesenchymal stem cell (MSC) and myeloid-derived suppressor cells (MDSCs) in a complex network of immune-endocrine signaling. The unique immunology of EMS is likely owing to estrogen dominance, as endocrine imbalance reliably cultivates immune dysregulation. Many of the phenomena observed in EMS parallel immune biology seen in various cancers, including accelerated somatic mutations in endometrial epithelial cells. Here, the high mutational load leads to EMS neoantigen development which potentially contributes to the lesion immune microenvironment. As well, EMS manifests comorbidity with several chronic inflammatory diseases that share common dysregulation of the interleukin-23 (IL-23)/IL-17 pathway (as seen in inflammatory bowel disease, psoriasis, and rheumatoid arthritis). EMS is especially relevant to the study of chronic pelvic pain (CPP) as 60% of EMS patients experience this symptom and chronic inflammation is believed to be central to the process of pain sensitization. Since the onset of the disease usually occurs in adolescence, and diagnosis only occurs years later once moderate to severe symptoms have developed, it is vital to innovate non-invasive diagnostic tools for earlier detection. Several potential biomarkers are being studied, including some cytokines, gene signatures, and extracellular vesicle (EV) signatures. By incorporating the immune perspectives of EMS into our research, approaches to diagnosis, and treatment solutions, the field has more promising avenues to clearly define EMS and offer patients relief.
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