Researchers designed a new therapy for multiple sclerosis by fusing a cytokine to a blood protein. In mice, this combination prevented destructive immune cells from infiltrating the central nervous system and decreased the number of cells that play a role in MS development, leading to fewer symptoms and even disease prevention. The results could lead to a new therapy for the disease.

While most immune cells help protect the body from disease, in patients with MS, autoreactive immune cells infiltrate the central nervous system and cause damage. Recent studies have shown Th17 cells – immune cells that are activated in the body's secondary lymphoid organs – migrate to the brain and play a role in the severity of the disease. Several drugs to treat MS work by sequestering these cells in the lymph nodes and preventing them from targeting tissue, but these drugs can have adverse side effects.
 
Interleukin-4, an anti-inflammatory cytokine, is known to suppress the genes that cause MS and has been found to suppress the reactivation of Th17 cells. To use it as a potential therapy, researchers needed to find a way to keep the IL-4 in the secondary lymphoid organs to ensure that Th17 cells were suppressed and did not migrate.
To do this, researchers at the Pritzker School of Molecular Engineering at the University of Chicago bound IL-4 to a blood protein and injected it into mice that had mouse model of MS and found that it caused the IL-4 to stay within the secondary lymphoid organs. The result was reduced infiltration of Th17 cells into the spinal cord. That suppressed the disease and resulted in fewer symptoms. Researchers found the therapy even prevented MS from developing in the majority of mice they treated with it.
 
Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. However, the therapy showed few negative side effects, and researchers will next formally study the toxicity of the therapy in hopes of eventually moving it to human clinical trials.

The findings were published in the journal Nature Biomedical Engineering.