Table 1.

Characteristics of M1 microglia and M2 microglia in ischemic stroke.

Phenotype	Markers	Mechanism	Effects
M1	CD16, CD32, CD86, IL-1β, IL-6, TNF-α, iNOS, MHCII, et al.	NF-κB is activated in microglia and transferred from cytoplasm to nucleus, activating the release of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α. TNF-α increases endothelial necrosis and BBB leakage	Proinflammatory, phagocytosis, cytotoxicity, present antigens, and kill intracellular pathogens
M2	CD206, Arg-1, TGF-β, CD163, IGF-1, IL-10, et al.	PParγ was activated in microglia and moved from nucleus to cytoplasm, resulting in the release of anti-inflammatory cytokines from M2. The up-regulation of TGF-α expression promoted the proliferation and neuronal differentiation of nerve stem/progenitor cells in the inferior ipsilateral ventricle	Anti-inflammatory, nerve repair, and tissue remodeling

CD, Cluster of Differentiation; IL, interleukin; TNF-α, Tumor necrosis factor-α; iNOS, Inducible nitric oxide synthase; MHCII, Major histocompatibility complex class II; Arg-1, Arginase-1; TGF-β, Transforming growth factor-β; IGF-1, Insulin growth factor 1.