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Type 1 diabetes risk can reliably be predicted by markers of autoimmunity, but approaches to prevent or modify the underlying disease process are needed. We posit this void fundamentally results from a limited understanding of immune-islet cell interactions within the pancreas and relevant immune organs, contributions of β-cells to their own demise, and epigenetic predispositions affecting both immune and islet cells. Because biopsy of the human pancreas and pancreatic lymph nodes carries risk and the pancreas begins to autodigest soon after death, detailed cellular and molecular phenotyping of the human type 1 diabetes pancreas is lacking, limiting our understanding of the mechanisms of β-cell loss. To address these challenges, the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases established the Human Pancreas Analysis Program (HPAP) to procure human type 1 diabetes pancreata for an extensive array of tissue-based, cellular, and epigenetic assays aimed at critical knowledge gaps in our understanding of the local immune attack and loss of β-cells. In this Methodology Review, we describe how HPAP is performing detailed islet and immune cell phenotyping and creating publicly available data sets with the goals of an improved understanding of type 1 diabetes and the development of more effective treatments to prevent or reverse the disease.
Pubmed ID: 31127054
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Network helps to organize and support collaborative research related to loss of functional beta cell mass in Type 1 Diabetes (T1D). Project consists of four independent research initiatives: Consortium on Beta Cell Death and Survival (CBDS), Consortium on Human Islet Biomimetics (CHIB), Consortium on Modeling Autoimmune Interactions (CMAI), Consortium on Targeting and Regeneration (CTAR), and Human Pancreas Analysis Program (HPAP).
View all literature mentionsProgram is performing deep phenotyping of human endocrine pancreas and its interaction with immune system to better understand cellular and molecular events that precede and lead to beta cell loss in Type-1 Diabetes (T1D) and islet dysfunction in Type-2 Diabetes (T2D).
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