T1D is caused by the autoimmune destruction of β-cells in the pancreas. Protein tyrosine phosphatases (PTPs) are T1D candidate genes that play an important role in developing autoimmune illness and β-cell dysfunction. For a study, researchers sought to determine the pancreas’ global protein and individual PTP profiles. The medication reduced hyperglycemia and increased the expression of PTPN2, a PTP family member and T1D candidate gene, and endoplasmic reticulum (ER) chaperones in the pancreatic islets. They created PTPN2-deficient human stem cell-derived β-like and EndoC-H1 cells to investigate the functional role of PTPN2 in β-cells.
They found that inactivating PTPN2 in β-cells exacerbates type I and type II interferon signaling networks and the potential development of autoimmunity. Furthermore, they found that PTPN2 may favorably affect the Ca2+-dependent unfolded protein response and the result of ER stress in β-cells. Overexpression of PTPN2 by adenovirus protected cells from ER stress-induced β-cell death. The findings supported the role of PTPN2 in β-cell protection during inflammation and ER stress in autoimmune diabetes.