Researchers Lorenzo Pasquali and Mireia Ramos-Rodríguez have published recently in Nature Genetics the results of a study on the mechanisms that cause an inflammatory response to trigger pancreatic beta-cell death, leading to the onset of Type 1 Diabetes (T1D). L. Pasquali is a Ramon y Cajal researcher at the Josep Carreras Leukaemia Research Institute (IJC), affiliated with CIBERDEM and the Germans Trias i Pujol Research Institute (IGTP), where he leads the Endocrine Regulatory Genomics group. Mireia Ramos-Rodríguez, the first author of the paper, is a doctoral student in the Endocrine Regulatory Genomics group. The study was carried out in collaboration with Decío Eizirik of ULB (Brussels, Belgium).
In T1D, the immune system selectively destroys pancreatic beta cells, depriving the capacity of this organ to produce insulin, and control blood sugar. In the search for why some people develop T1D, researchers have identified more than 60 regions on the genome where there are genetic variants associated with a higher risk of developing T1D, but their functions are not known yet. Additionally, most of these variants locate in DNA sequences that don’t encode proteins and are dismissed as “junk DNA.”
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