Alberto Pugliese, Mingder Yang, Irina Kusmarteva, Tiffany Heiple, Francesco Vendrame, Clive Wasserfall, Patrick Rowe, Jayne M Moraski, Suzanne Ball, Les Jebson, Desmond A Schatz, Roberto Gianani, George W Burke, Concepcion Nierras, Teo Staeva, John S Kaddis, Martha Campbell-Thompson, Mark A Atkinson

nPOD actively promotes a multidisciplinary and unbiased approach toward a better understanding of T1D and identify novel therapeutic targets, through its focus on the study of human samples. Unique to this effort is the coordination of collaborative efforts and real-time data sharing. Studies supported by nPOD are providing direct evidence that human T1D isa complex and heterogeneous disease, in which a multitude of pathogenic factors may be operational and may contribute to the onset of the disease. Importantly, the concept that beta cell destruction is almost completed and that the autoimmune process is almost extinguished soon after diagnosis is being challenged. nPOD investigators are exploring the hypothesis that beta cell dysfunction may also be a significant cause of hyperglycemia, at least around the time of diagnosis, and are uncovering novel molecules and pathways that are linked to the pathogenesis and etiology of human T1D. The validation of therapeutic targets is also a key component of this effort, with recent and future findings providing new strategic direction for clinical trials.