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Review
. 2016:2016:8489251.
doi: 10.1155/2016/8489251. Epub 2016 Mar 13.

Double Roles of Macrophages in Human Neuroimmune Diseases and Their Animal Models

Xueli Fan  1 , Hongliang Zhang  1 , Yun Cheng  1 , Xinmei Jiang  1 , Jie Zhu  2 , Tao Jin  1
Affiliations
Review

Double Roles of Macrophages in Human Neuroimmune Diseases and Their Animal Models

Xueli Fan et al. Mediators Inflamm. 2016.

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.

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Figures

Figure 1
Figure 1
Origin and self-renewal of macrophage. Tissue macrophages have dual origins. One part develops from embryonic progenitors in the yolk sac and fetal liver and self-renew. The other part derives from hematopoietic stem cells (HSCs) in bone marrow and blood monocyte intermediates. HSCs also can self-replenish themselves. Monocyte-derived macrophages can give rise to some subsets of resident macrophages under certain conditions. Resident macrophages and monocyte-derived macrophages ultimately constitute macrophages in all tissues, such as microglia in the brain, Langerhans cells in the skin, and Kupffer cells in the liver. EMPs, erythromyeloid progenitors; HSCs, hematopoietic stem cells.
Figure 2
Figure 2
Macrophage polarization into proinflammatory and anti-inflammatory macrophages. Macrophages polarize and acquire different functional properties in response to numerous factors from the microenvironment. Macrophages activated by IFN-γ, LPS, or TNF-α can develop proinflammatory macrophages, with strong microbicidal and tumoricidal properties. In contrast, anti-inflammatory macrophages contribute to Th2 response, immunoregulation, and tissue remodeling. Anti-inflammatory macrophages have different subsets. M(IL-4) macrophages (induced by exposure to IL-4) secret TNF-α, IL-1, and IL-6 and induce Th2 cell response and allergy. M(IC) macrophages (induced by IC) secret IL-10 and exert immunoregulatory function. M(IL-10) macrophages (induced by IL-10) secret IL-10 and TGF-β, suppress immune responses, and promote tissue remodeling. CCL, CC-chemokine ligand; CXCL, CXC-chemokine ligand; IC, immune complexes; IFN-γ, interferon γ; LPS, lipopolysaccharide; MHC-II, major histocompatibility complex-II; MR, mannose receptor; NO, nitric oxide; ROI, reactive oxygen intermediates; SLAM, signaling lymphocytic activation molecule; SR, scavenger receptor; TGF-β, transforming growth factor-β; TLR, toll-like receptor; TNF-α, tumor necrosis receptor-α.
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