Researchers from Tufts University School of Medicine and Tufts Graduate School of Biomedical Sciences aimed to investigate the immune system’s role in doxorubicin-induced heart damage. The study found that doxorubicin can damage the heart by creating harmful molecules called reactive oxygen species (ROS). These molecules trigger inflammation, involving immune cells such as CD4+ and CD8+ T cells.
Normally, these cells defend the body against infections and tumors. However, researchers discovered that doxorubicin can cause these defenders to attack the heart. Experiments on mice showed that doxorubicin treatment increased CD8+ T cells in the heart.
CD8+ T cells produce inflammatory substances that cause heart tissue damage and scarring, decreasing the heart’s ability to pump blood effectively. When the researchers removed the CD8+ T cells from the mice, the heart damage and scarring were significantly reduced. This immune response was not limited to mice.
The study also included observations from dogs and humans. Both groups showed increased levels of CD8+ T cells after receiving doxorubicin, linking the drug to immune-triggered heart damage across different species. “Our study is the first to show that a specific cell type can cause chronic inflammation in the heart after doxorubicin treatment and the first time T-cells have been implicated in this disease,” study author Abe Bayer, a student in the Tufts M.
D./Ph.D.
immunology program, said in a press release. The resea.