Department of Ophthalmology, Nippon Medical School, Tama-Nagayama Hospital, Tokyo 2068512, Japan.
Int J Mol Sci. 2021 Dec 29;23(1):341. doi: 10.3390/ijms23010341.
Scleritis involves inflammation of the sclera, which constitutes 75% of the wall of the eye. This pathology is often seen as an ocular lesion associated with systemic inflammatory diseases. Severe types of scleritis such as posterior scleritis require urgent immunosuppressive treatments, including molecularly targeted therapies to avoid permanent visual impairment. Which molecules should be selected as targets has remained unclear. To clarify the pathogenesis of scleritis and propose appropriate target molecules for therapy, we have established novel animal model of scleritis by modifying the Collagen-II Induced Arthritis (CIA) model. Immunization twice with collagen II emulsified with complete Freund's adjuvant (CFA) caused arthritis and scleritis. The clinical appearance resembled human diffuse scleritis. Histopathological analysis suggested that macrophages, plasma cells, deposition of immune complexes, and growth of blood and lymphatic vessels are involved in the pathogenesis of CIA-associated scleritis. In addition, we analysed the background diseases of posterior scleritis and responses to molecularly targeted therapies as a case series study. We inferred from both the animal model and case series study that targets should not be T cells, but factors inhibiting macrophage activity such as tumor necrosis factor (TNF) and interleukin (IL)-6, and molecules suppressing antibody-producing cells such as CD20 on B cells should be targeted by molecularly targeted therapies.
巩膜炎涉及巩膜炎症,巩膜构成了眼球壁的 75%。这种病理学通常被视为与全身性炎症性疾病相关的眼部病变。严重的巩膜炎类型,如后巩膜炎,需要紧急免疫抑制治疗,包括分子靶向治疗,以避免永久性视力损害。哪些分子应作为靶点仍然不清楚。为了阐明巩膜炎的发病机制并为治疗提出合适的靶分子,我们通过修改胶原诱导性关节炎(CIA)模型建立了新型巩膜炎动物模型。用完全弗氏佐剂(CFA)乳化的胶原 II 进行两次免疫接种会导致关节炎和巩膜炎。临床外观类似于人类弥漫性巩膜炎。组织病理学分析表明,巨噬细胞、浆细胞、免疫复合物沉积以及血液和淋巴管的生长都参与了 CIA 相关巩膜炎的发病机制。此外,我们还进行了一项病例系列研究,分析了后巩膜炎的基础疾病和对分子靶向治疗的反应。我们从动物模型和病例系列研究中推断,靶点不应该是 T 细胞,而是抑制巨噬细胞活性的因子,如肿瘤坏死因子(TNF)和白细胞介素(IL)-6,以及抑制 B 细胞产生抗体的细胞的分子,如 CD20,应该成为分子靶向治疗的靶点。