Jarrah, Abdul SalamCastiglione, FilippoEvans, Nicholas P.Grange, Robert W.Laubenbacher, Reinhard C.2017-09-182017-09-182014-06-11Abdul Salam Jarrah, Filippo Castiglione, Nicholas P. Evans, Robert W. Grange, and Reinhard Laubenbacher, “A Mathematical Model of Skeletal Muscle Disease and Immune Response in the mdx Mouse,” BioMed Research International, vol. 2014, Article ID 871810, 11 pages, 2014. doi:10.1155/2014/871810http://hdl.handle.net/10919/78960Duchenne muscular dystrophy (DMD) is a genetic disease that results in the death of affected boys by early adulthood. The genetic defect responsible for DMD has been known for over 25 years, yet at present there is neither cure nor effective treatment for DMD. During early disease onset, the mdx mouse has been validated as an animal model for DMD and use of this model has led to valuable but incomplete insights into the disease process. For example, immune cells are thought to be responsible for a significant portion of muscle cell death in the mdx mouse; however, the role and time course of the immune response in the dystrophic process have not been well described. In this paper we constructed a simple mathematical model to investigate the role of the immune response in muscle degeneration and subsequent regeneration in the mdx mouse model of Duchenne muscular dystrophy. Our model suggests that the immune response contributes substantially to the muscle degeneration and regeneration processes. Furthermore, the analysis of the model predicts that the immune system response oscillates throughout the life of the mice, and the damaged fibers are never completely cleared.application/pdfenCreative Commons Attribution 4.0 InternationalA Mathematical Model of Skeletal Muscle Disease and Immune Response in the mdx MouseArticle - Refereed2017-09-18Copyright © 2014 Abdul Salam Jarrah et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.BioMed Research Internationalhttps://doi.org/10.1155/2014/871810