Double Roles of Macrophages in Human Neuroimmune Diseases and Their Animal Models.
Double Roles of Macrophages in Human Neuroimmune Diseases and Their Animal Models.
复制标题
巨噬细胞在人类神经免疫疾病及其动物模型中的双重作用。
DOI：
10.1155/2016/8489251
复制
发表时间：
2016
影响因子：
4.6
通讯作者：
Jin T
中科院分区：
文献类型：
--
作者：
Fan X;Zhang H;Cheng Y;Jiang X;Zhu J;Jin T
巨噬细胞是先天免疫系统的重要免疫细胞，其参与器官特异性稳态，并有助于疾病的病理学和解决，包括感染、癌症、肥胖、动脉粥样硬化和自身免疫性疾病。多种证据表明巨噬细胞是一种非常异质的细胞类型。不同表型的巨噬细胞发挥促炎或抗炎作用，这取决于它们在局部微环境中暴露于的细胞因子和其他介质。促炎性巨噬细胞分泌有害分子以诱导疾病发展，而抗炎性巨噬细胞产生有益介质以促进疾病恢复。巨噬细胞表型的转换可以调节自身免疫性疾病的发生、发展和恢复。人类神经免疫性疾病主要包括多发性硬化症（MS）、视神经肌萎缩症（NMO）、重症肌无力（MG）和格林-巴利综合征（GBS），巨噬细胞参与这些神经免疫性疾病的发病机制。本文就巨噬细胞在神经免疫性疾病中的双重作用及其动物模型进行综述，旨在进一步探讨巨噬细胞参与神经免疫性疾病发病机制，为神经免疫性疾病的治疗提供新的思路。
Macrophages are important immune cells of the innate immune system that are involved in organ-specific homeostasis and contribute to both pathology and resolution of diseases including infections, cancer, obesity, atherosclerosis, and autoimmune disorders. Multiple lines of evidence point to macrophages as a remarkably heterogeneous cell type. Different phenotypes of macrophages exert either proinflammatory or anti-inflammatory roles depending on the cytokines and other mediators that they are exposed to in the local microenvironment. Proinflammatory macrophages secrete detrimental molecules to induce disease development, while anti-inflammatory macrophages produce beneficial mediators to promote disease recovery. The conversion of the phenotypes of macrophages can regulate the initiation, development, and recovery of autoimmune diseases. Human neuroimmune diseases majorly include multiple sclerosis (MS), neuromyelitis optica (NMO), myasthenia gravis (MG), and Guillain-Barré syndrome (GBS) and macrophages contribute to the pathogenesis of these neuroimmune diseases. In this review, we summarize the double roles of macrophage in neuroimmune diseases and their animal models to further explore the mechanisms of macrophages involved in the pathogenesis of these disorders, which may provide a potential therapeutic approach for these disorders in the future.