effect is the induction of M2 microglia. Additionally, other M2 promoting cytokines, such as IL-33 [98] and IL-10 [96], have been shown to reduce the amount of demyelination [96] and improve clinical scores [98]. It is important to note that these EAE models were of the chronic variety, as opposed to other EAE models that only display a transient pathology. This demonstrates that altering the pro-M1 environment to one more conducive to M2 generation has beneficial effects in chronic diseases (Table 2). The mechanism behind the beneficial effects of M2 cells can be attributed to their production of neurotropic mediators that support remyelination and regeneration. Factors such as IGF1, PDGFα, TGFβ, and SPP1 are all upregulated in microglia during the recovery phase of disease [112].
