Scientists at the Institute of Experimental Immunology at the University of Zurich have found that autophagy proteins are responsible for triggering autoimmune processes in a mouse model of multiple sclerosis. The work was published in Proceedings of the National Academy of Sciences yesterday.
In this study, the researchers led by Jan Lünemann genetically turned off the autophagy protein ATG5 in certain immune cells. By doing this, they saw less pathological T cells in the central nervous system in mice. The animals failed to develop inflammation in the brain and spinal cord comparable with inflammation that develops in multiple sclerosis.
From this study, the researchers have shown that ATG5 is essential when myelin antigens are presented to immune cells during inflammation processes in the central nervous system. "This reactivation process is thought to play a decisive role in the development of autoimmune neuroinflammation," says Christian Keller, lead author of the study.
The team plans to move forward and use their findings as a basis for investigating tissue samples of patients suffering from multiple sclerosis to find out whether autophagy is particularly active in certain immune cells. "In the long run, we want to see whether these new immunopathology findings can be used to develop new treatments for multiple sclerosis," says Lünemann.