M1-like macrophages are represented by surface expression of Ly6C and MHC-II and gene expression of Nlrp3, Il1b, Tnf, and Nos2. M1-like macrophages are induced by such factors as FFAs, hIAPPs, and endocannabinoids, and at least some M1-like macrophages are recruited through CCL2 signaling. M2-like macrophages are represented by surface expression of CD206 and CD301 and gene expression of Il10, Arg1, and Tgfb1. At least some M2-like macrophages self-renew or are recruited through CSF1 signaling. In the sterile islet inflammation observed in T2D, islet macrophages’ polarization is seamlessly regulated as a continuum, rather than as distinct bimodal M1 and M2 polarization. Studies of the regulation of islet macrophage polarization, characterizations of subsets of heterogeneous islet macrophages, and analyses of the mechanisms by which these polarized macrophages exert their physiologic and pathologic effects on islet biology have the potential for translation to T2D therapeutics.