The recent advances in our understanding of alternatively activated microglia and their potential efficacy in treating disease have led to greater interest in translational human studies. Unfortunately, the leap to human M2 cells is not without its own problems. As noted in Table 1, several commonly used markers, such as Arg1 and YM1 are not expressed in human myeloid cells [33], which limits the ability to identify distinct human microglial phenotypes. However, other markers appear to be consistent. CD163-positive cells have been observed in stroke and multiple sclerosis, providing a means to identify M2 microglia in human diseases [39,157]. Furthermore, mutations in TREM2, a molecule implicated in both human and murine M2 microglial function, are associated with increased risk of Alzheimer’s disease [158]. In relation to this idea, levels of M2-inducing molecules, such as resolvin D1 [21,159] and IL-10, were reduced in patients with Alzheimer’s disease [160]. Moreover, resolvin D1 levels significantly correlated with worse Mini-Mental State Examination scores [160], suggesting that the lack of factors to induce M2 polarization has potential functional relevance in human disease. To that end,
