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Figure 3 In the context of T1D, the populations of resident islet macrophages in both animal models and humans display an pro-inflammatory phenotype, characterized by the secretion of cytokines (such as IL-1β and TNF), upregulated expression of MHC-II and increased antigen presentation capacity, and decreased phagocytosis of apoptotic β-cells ( Furthermore, monocyte-derived macrophages are among the first, and most abundant, immune cells to traffic into the islet in both murine models and human patients ( This inflammatory environment can be exacerbated by priming factors that mediate crosstalk between macrophages and β-cells