Izuka Shinji, Komai Toshihiko, Tsuchida Yumi, Tsuchiya Haruka, Okamura Tomohisa, Fujio Keishi
Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Department of Functional Genomics and Immunological Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Front Immunol. 2025 Mar 20;16:1567833. doi: 10.3389/fimmu.2025.1567833. eCollection 2025.
Idiopathic inflammatory myopathies (IIMs) are heterogeneous autoimmune disorders characterized by muscle inflammation, weakness, and extramuscular manifestations such as interstitial lung disease, skin rash, arthritis, dysphagia, myocarditis and other systemic organ involvement. Although T and B cells have historically been central to the understanding of IIM immunopathology, monocytes and their differentiated progenitor cells, macrophages, are increasingly being recognized as critical mediators of both tissue damage and repair. In subtypes such as dermatomyositis, immune-mediated necrotizing myopathy and antisynthetase syndrome, macrophages infiltrate skeletal muscle and other affected tissues, contributing to inflammation via production of pro-inflammatory cytokines, chemokines, and reactive oxygen species. Dysregulated interferon signaling, mitochondrial stress, and aberrant metabolic states in these cells further perpetuate tissue injury in IIMs. Conversely, certain macrophage subsets can support muscle fiber regeneration and dampen inflammation, underscoring the dual roles these cells can play. Future research into the heterogeneity of monocytes and macrophages, including single-cell transcriptomic and metabolomic approaches, will help clarify disease mechanisms, identify biomarkers of disease activity and prognosis, and guide novel therapeutic strategies targeting these innate immune cells in IIM.
特发性炎性肌病(IIMs)是一类异质性自身免疫性疾病,其特征为肌肉炎症、肌无力以及诸如间质性肺疾病、皮疹、关节炎、吞咽困难、心肌炎和其他全身器官受累等肌肉外表现。尽管传统上T细胞和B细胞一直是理解IIM免疫病理学的核心,但单核细胞及其分化的祖细胞——巨噬细胞,正日益被视为组织损伤和修复的关键介质。在皮肌炎、免疫介导的坏死性肌病和抗合成酶综合征等亚型中,巨噬细胞浸润骨骼肌和其他受累组织,通过产生促炎细胞因子、趋化因子和活性氧来促进炎症。这些细胞中失调的干扰素信号传导、线粒体应激和异常代谢状态进一步使IIMs中的组织损伤持续存在。相反,某些巨噬细胞亚群可支持肌纤维再生并减轻炎症,凸显了这些细胞可发挥的双重作用。未来对单核细胞和巨噬细胞异质性的研究,包括单细胞转录组学和代谢组学方法,将有助于阐明疾病机制、识别疾病活动和预后的生物标志物,并指导针对IIM中这些固有免疫细胞的新型治疗策略。