A New Strategy for Treating Autoimmune Disease While Maintaining Immune Function

Although scientists have made considerable progress in treating autoimmune diseases such as type 1 diabetes and multiple sclerosis, few available treatments can stop or reverse disease progression. In addition, existing therapies cause chronic immune deficiency, limiting their usefulness. University of Utah Health investigator Mingnan Chen, PhD, and colleagues in the Department of Molecular Pharmaceutics have discovered a new therapeutic strategy that avoids immune deficiency while treating autoimmune disease. Specifically, they identified immune cells that express a key immune checkpoint receptor that drives type 1 diabetes and multiple sclerosis. The Chen lab then created an immunotoxin that selectively depletes these cells. Treatment with the immunotoxin reverses the progression of a mouse version of multiple sclerosis and delays the onset of type 1 diabetes in mice. This treatment has two distinct advantages: it targets multiple types of autoimmune disease-causing cells, but also leaves the majority of immune cells intact after the targeted depletion. Thus, it does not cause broad immune deficiency. The treatment opens new horizons in treating autoimmune diseases.