Table 2.

Roles of different functional subpopulations of macrophages in MS and EAE.

	Tissue resident macrophages  (microglia)	Monocyte-derived macrophages	Proinflammatory macrophages	Anti-inflammatory macrophages	Refs
MS	As competent APCs  Secretion of proinflammatory and neurotoxic molecules     Maintenance of CNS homeostasis  Immunosuppression	Eating myelin remnants  Secreting proinflammatory cytokines     Displaying an intermediate activation to suppress neuroinflammation and promote CNS repair	Excessive secretion of proinflammatory cytokines, ROI and NO	Phagocytosing debris  Promoting tissue repair  Increased anti-inflammatory macrophages in MS after treatment with glatiramer acetate	[66–77]
EAE	Promoting the development and inflammatory lesions in CNS in the early stage of EAE    Eliminating debris and suppressing cellular metabolism at EAE onset  Secretion of TGF-β to induce a protective process	Presenting antigen  Activating myelin-reactive T cells  Expressing adhesion molecules and chemokines to attract leukocyte infiltration into CNS  Activating some microglia to accelerate inflammation	Contributing to the establishment of early inflammation in EAE  Associating with EAE severity	Promoting the differentiation of Th2 cells and Tregs to suppress EAE severity  Inhibiting the development of Th17 cells	[30, 36, 37, 78–86]

APCs, antigen presenting cells; CNS, central nervous system; EAE, experimental autoimmune encephalomyelitis; MS, multiple sclerosis; NO, nitric oxide; ROI, reactive oxygen intermediates; TGF-β, transforming growth factor-β; Th2, T helper 2; Th17, T helper 17; Tregs, regulatory T cells.