As alterations in autophagic flux may contribute to T1D, we are seeking to determine if particular lysosomal components of beta cell autophagy participate in or dysregulate this essential process. The focus of this addendum is on the enzyme cathepsin H as specific genetic variants in this gene have been identified as T1D–associated SNPs. Through these studies, we will better define whether T1D-susceptible variants of genes encoding lysosomal enzymes modulate markers of autophagy in human pancreas tissue.
