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Type 1 and type 2 diabetes (T1D and T2D) are generally recognized as distinct disease entities based on the mechanism of induction of disease: T1D results from low or no insulin production due to the gradual loss of cells that produce insulin, whereas T2D is generally thought to occur as a result of the body’s development of resistance to insulin. Although the events initiating T1D and T2D might be very different, the progression to diabetes and complications are similar and involve interactions between the immune system and the metabolic system. Notably, chronic inflammation is a shared manifestation of the two types of diabetes (1,2). Recently, secreted microvesicles, particularly exosomes, were suggested to be intermediates linking inflammation to diabetes (3). The cellular origins of the vesicles and the genetic and environmental factors that cause an abnormal production of the vesicles are likely to be central in linking the inflammation to tissue-specific damage. For example, islet mesenchymal stem cells from autoimmune-prone animals were shown to release highly proinflammatory exosomes that contributed to T1D (4), and the low-grade inflammation in obesity may stimulate release of proinflammatory microvesicles and exosomes to accelerate T2D (5,6). “Extracellular vesicles” (EVs) is a collective term for different types of small-sized membrane vesicles or particles that are secreted by cells, including exosomes, microvesicles, apoptotic bodies, and virus-like particles. Figure 1 shows a generalization of their similarities and differences in biogenesis and immune-stimulatory function. There are many reasons that such organelles may be produced, including packaging of paracrine factors for intercellular communications, apoptosis resulting from breakdown of cells, and packaging of material for ingestion and disposal by scavenger cells (7). Viruses too have learned to take advantage of the vesicle biogenesis machinery to hide from immune surveillance to establish infections at immune-privileged sites …