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Type 1 diabetes is conventionally thought to result from T-cell–mediated autoimmune destruction of pancreatic β-cells (1–3). Experimental and clinical evidence accumulated over the past two decades indicates that T-cells play a critical role in the pathogenesis of type 1 diabetes in both humans and the nonobese diabetic (NOD) mouse model of this disease (4). Indeed, the important contribution of T-cells toward the pathogenesis of type 1 diabetes has been supported not only by a variety of physiologic and histological studies but, in addition, through a number of immunotherapeutic-based studies involving selective targeting of T-cells (4,5). More recently, it has been shown that B-cells also play an important role in type 1 diabetes development (6), since NOD mice deficient in these cells do not develop insulitis or overt diabetes (7), and that the depletion of B-cells with anti-CD20 antibody prevents disease (8).Apart from diabetogenic T- and B-cells, emerging evidence suggests that macrophages are involved in the final stage of autoimmune-mediated β-cell destruction (9,10). For example, after monocyte depletion, passively transferred diabetogenic T-cells fail to induce diabetes, and activated macrophages can directly kill β-cells in vitro (10). However, direct evidence that activated monocytes/macrophages kill β-cells is minimal or lacking, depending on one's perspective. In the current issue of Diabetes , Martin et al. …

Big Mac Attack: Does It Play a Direct Role for Monocytes/Macrophages in Type 1 Diabetes?