Abstract: Activated iNKT cells act as senolytic agents, removing senescent cells from target tissues, organs, and compartments of the body. Provided are methods of clearing pathological accumulations of senescent cells by administration of iNKT cell activators such as an alpha-galactosylceramide, or variants or by the adoptive transfer of iNKT cells or precursors, enabling the treatment of senescence-associated conditions such as diabetes, lung fibrosis, and other conditions.

Abstract: The inventor of the present disclosure has advantageously elucidated the role of senescent processes in the development of Type 1 diabetes. Genotoxic stress responses, senescence, and acquisition of a SASP condition in beta cells are drivers that progress at-risk individuals to overt Type 1 diabetes. The administration of senolytic agents to at risk individuals selectively removes senescent cells and relieves beta cells from the factors which drive the development of overt Type 1 diabetes. Accordingly, Type 1 diabetes can be prevented in at-risk individuals by the administration of senolytic compositions. Additionally, given the major role of SASP in the development of Type 1 diabetes, the inhibition of SASP factors may be used to prevent Type 1 diabetes.

Abstract: The inventor of the present disclosure has advantageously elucidated the role of senescent processes in the development of Type 1 diabetes. Genotoxic stress responses, senescence, and acquisition of a SASP condition in beta cells are drivers that progress at-risk individuals to overt Type 1 diabetes. The administration of senolytic agents to at risk individuals selectively removes senescent cells and relieves beta cells from the factors which drive the development of overt Type 1 diabetes. Accordingly, Type 1 diabetes can be prevented in at-risk individuals by the administration of senolytic compositions. Additionally, given the major role of SASP in the development of Type 1 diabetes, the inhibition of SASP factors may be used to prevent Type 1 diabetes.

Abstract: A method of facilitating the proliferation of pancreatic progenitor cells, particularly mammalian cells, is described. The method is carried out by administering an FGF polypeptide such as FGF-10 polypeptide to the cells in an amount effective to facilitate the proliferation thereof.