title: Double Roles of Macrophages in Human Neuroimmune Diseases and Their Animal Models.
abstract: 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.
authors.affiliation: Department of Neurology and Neuroscience Center, First Hospital of Jilin University, Jilin University, Changchun 130021, China.
authors.forename: Xueli
authors.initials: X
authors.lastname: Fan
authors.affiliation: Department of Neurology and Neuroscience Center, First Hospital of Jilin University, Jilin University, Changchun 130021, China.
authors.forename: Hongliang
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Neurology and Neuroscience Center, First Hospital of Jilin University, Jilin University, Changchun 130021, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Cheng
authors.affiliation: Department of Neurology and Neuroscience Center, First Hospital of Jilin University, Jilin University, Changchun 130021, China.
authors.forename: Xinmei
authors.initials: X
authors.lastname: Jiang
authors.affiliation: Department of Neurology and Neuroscience Center, First Hospital of Jilin University, Jilin University, Changchun 130021, China; Department of Neurobiology, Care Sciences and Society, Karolinska Institute, 141 86 Stockholm, Sweden.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Department of Neurology and Neuroscience Center, First Hospital of Jilin University, Jilin University, Changchun 130021, China.
authors.forename: Tao
authors.identifier: 0000-0002-7028-3419
authors.initials: T
authors.lastname: Jin
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology / Q000378:metabolism*; D004195:Disease Models, Animal; D020275:Guillain-Barre Syndrome / Q000276:immunology / Q000378:metabolism; D006801:Humans; D008264:Macrophages / Q000276:immunology / Q000378:metabolism*; D009103:Multiple Sclerosis / Q000276:immunology / Q000378:metabolism; D009157:Myasthenia Gravis / Q000276:immunology / Q000378:metabolism; D009471:Neuromyelitis Optica / Q000276:immunology / Q000378:metabolism