Current treatment regimens for autoimmune diseases indiscriminately target healthy and diseased immune cells, causing patient immunodeficiency. In disorders like type 1 diabetes, multiple sclerosis, and rheumatoid arthritis, there is systemic depletion of healthy cells and tissues due to the failure of regulatory checkpoints in the immune system, like the PD-1 receptor.
University of Utah researchers have developed a unique approach to specifically deplete pathogenic autoreactive immune cells that cause organ destruction. This approach uses a targeted therapeutic with a PD-1-receptor-targeting moiety conjugated to a unique exotoxin. The exotoxin enters only offending autoimmune cells to begin depletion, without targeting or affecting healthy cells. This approach has been shown to limit healthy cell exposure to the toxin and reduce autoimmune deficiency in mouse models for type 1 diabetes and experimental autoimmune encephalomyelitis.