Scientists developed a new therapy for multiple sclerosis (MS) that prevents immune cells from exiting the lymph nodes and entering the spinal cord of mice with experimental autoimmune encephalomyelitis (EAE) — a condition that mimics MS in humans.
The therapy, which consists of a molecule resulting from the fusion of a blood protein and an anti-inflammatory signaling molecule, also lowered the number of a subset of immune T-cells that are thought to play a key role in the disease. The treatment also reduced MS symptoms and even prevented the disease in mice.
“The exciting result is that we can suppress MS symptoms in a way that is more effective than current treatments,” Jeffrey Hubbell, PhD, co-author of the study and professor in tissue engineering at the Pritzker School of Molecular Engineering (PME) at the University of Chicago, said in a press release.
The findings were reported in the study, “Prolonged residence of an albumin–IL-4 fusion protein in secondary lymphoid organs ameliorates experimental autoimmune encephalomyelitis,” published in the journal Nature Biomedical Engineering.
MS is an autoimmune disease resulting from the excessive activity of pro-inflammatory immune cells that travel to the brain and spinal cord, where they attack the myelin sheath that insulates and protects nerve fibers, leading to neurodegeneration.
Some medications currently used to manage the disease, including Gilenya (fingolimod) and Tysabri (natalizumab), work by preventing these self-reactive immune cells from entering the central nervous system (CNS), which is composed of the brain and spinal cord. However, these therapies can cause several side effects.
Thus, researchers have now developed and validated a new form of therapy that may be even more effective than current treatments at keeping MS symptoms at bay.
The team of scientists created a hybrid molecule by binding interleukin-4, or IL-4, to a blood protein called albumin. IL-4 is an anti-inflammatory molecule that has been shown to suppress the differentiation and reactivation of a subtype of pro-inflammatory T-helper cells, called Th17, which have been implicated in MS.
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