Extracellular vesicles derived from stressed beta cells mediate monocyte activation and contribute to islet inflammation.

ABSTRACT:

Objective

Beta cell destruction in type 1 diabetes (T1D) results from the combined effect of inflammation and recurrent autoimmunity. In recent years, the role played by beta cells in the development of T1D has evolved from passive victims of the immune system to active contributors in their own destruction. We and others have demonstrated that perturbations in the islet microenvironment promote endoplasmic reticulum (ER) stress in beta cells, leading to enhanced immunogenicity. Among the underlying mechanisms, secretion of extracellular vesicles (EVs) by beta cells has been suggested to mediate the crosstalk with the immune cell compartment.

Methods

To study the role of cellular stress in the early events of T1D development, we generated a novel cellular model for constitut

SUBMITTER: Dekkers MC 

PROVIDER: S-EPMC11303142 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature