摘要
葡萄膜炎是一些潜在威胁视力的眼内炎症疾病,由感染或自身免疫病引起。美国此种眼科疾病发病率占严重视力障碍的10%。此种眼科疾病的病理学是源于光轴炎性细胞和具有细胞毒性的细胞因子及眼部其他免疫调节蛋白持续产生。主要治疗目标是使免疫反应下调,保持眼球结构的完整性和最终消除葡萄膜炎性基因的刺激。目前的治疗方法是使用二线药物辅助或不辅助来进行局部或全身性糖皮质激素治疗,由于这些药物产生严重不良反应,进而推动了对葡萄膜炎症低毒及更强特异性治疗方法的研究。本文综述了葡萄膜炎症的病理生理机制,调节葡萄膜炎症发病的分子机制,并为潜在致盲疾病的治疗总结了新方法。
关键词: B细胞治疗,细胞因子IL-12,IL-35表达的Breg细胞(i35 Breg),白细胞介素35(IL-35),调节性B细胞(Breg),细胞因子治疗,葡萄膜炎。
Current Molecular Medicine
Title:Ocular Inflammatory Diseases: Molecular Pathogenesis and Immunotherapy
Volume: 15 Issue: 6
Author(s): 眼部炎症性疾病:分子发病机制与免疫疗法
Affiliation:
关键词: B细胞治疗,细胞因子IL-12,IL-35表达的Breg细胞(i35 Breg),白细胞介素35(IL-35),调节性B细胞(Breg),细胞因子治疗,葡萄膜炎。
摘要: Uveitis is a diverse group of potentially sight-threatening intraocular inflammatory diseases of infectious or autoimmune etiology and accounts for more than 10% of severe visual handicaps in the United States. Pathology derives from the presence of inflammatory cells in the optical axis and sustained production of cytotoxic cytokines and other immuneregulatory proteins in the eye. The main therapeutic goals are to down-regulate the immune response, preserve the integrity of the ocular architecture and eventually eliminate the inciting uveitogenic stimuli. Current therapy is based on topical or systemic corticosteroid with or without second line agents and serious adverse effects of these drugs are the impetus for development of less toxic and more specific therapies for uveitis. This review summarizes the pathophysiology of uveitis, molecular mechanisms that regulate the initiation and progression of uveitis and concludes with emerging strategies for the treatment of this group of potentially blinding diseases.
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Cite this article as:
眼部炎症性疾病:分子发病机制与免疫疗法 , Ocular Inflammatory Diseases: Molecular Pathogenesis and Immunotherapy, Current Molecular Medicine 2015; 15 (6) . https://dx.doi.org/10.2174/1566524015666150731095426
DOI https://dx.doi.org/10.2174/1566524015666150731095426 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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