UC Merced

Autoimmune disease is driven by the dysregulation of one’s own immune system and its inability to distinguish self-antigens from foreign; however, the etiology of autoimmunity is not wholly understood. To shed light on this complex condition, we have developed a mathematical model that captures the dynamics of autoimmune disease development. The model is based on data obtained from experiments on BALB/c mice, both wildtype and autoimmune mice deficient in interleukin-2. This study focuses on the interactions between naive CD4 T cells, regulatory CD4 T cells, activated CD4 T cells, and the dynamic influence of IL-2 on Treg functionality and survival. Our model provides a quantitative understanding of the differences between healthy and autoimmune immune systems and identifies potential targets for therapeutic intervention. To the best of our knowledge, this is the first published mathematical model that explores early immune development in IL-2 knockout mice and the dynamics of immune cells that prevent autoimmune disease.