/blog/multiple-sclerosis-an-autoimmune-disease-of-the-central-nervous-system-that-affects-millions-worldwide-can-cause-debilitating-symptoms-for-those-who-suffer-from-it Another great news in Medical Research today is that MS symptoms can be suppressed in a way that is more effective than current treatments.
Multiple sclerosis, an autoimmune disease of the central nervous system that affects millions worldwide, can cause debilitating symptoms for those who suffer from it.
Though treatments exist, researchers are still searching for therapies that could more effectively treat the disease, or even prevent it altogether.
Researchers at the Pritzker School of Molecular Engineering (PME) at the University of Chicago have designed a new therapy for multiple sclerosis (MS) 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.
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 that 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 (IL-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, they bound IL-4 to a blood protein and injected it into mice that had experimental autoimmune encephalomyelitis (the 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. Medical research done in University of Chicago has found that the newly designed therapy by PME researcher can prevent MS from developing in the majority of mice it was treated with. This therapy if moved to clinical trial could potentially be self-administered by MS patients at home with an injector pen and could lead to better quality of life, with fewer symptoms, for those with the disease
This is a big breakthrough given that it is the first time anyone has shown how the fusion of this protein to immunosuppressive cytokines can treat and prevent multiple sclerosis.
Medical research procedure
Prolonged residence of an albumin–IL-4 fusion protein in secondary lymphoid organs ameliorates experimental autoimmune encephalomyelitis
nterleukin-4 (IL-4) suppresses the development of multiple sclerosis in a murine model of experimental autoimmune encephalomyelitis (EAE). Here, we show that, in mice with EAE, the accumulation and persistence in the lymph nodes and spleen of a systemically administered serum albumin (SA)–IL-4 fusion protein leads to higher efficacy in preventing disease development than the administration of wild-type IL-4 or of the clinically approved drug fingolimod. We also show that the SA–IL-4 fusion protein prevents immune-cell infiltration in the spinal cord, decreases integrin expression in antigen-specific CD4+ T cells, increases the number of granulocyte-like myeloid-derived suppressor cells (and their expression of programmed-death-ligand-1) in spinal cord-draining lymph nodes and decreases the number of T helper 17 cells, a pathogenic cell population in EAE. In mice with chronic EAE, SA–IL-4 inhibits immune-cell infiltration into the spinal cord and completely abrogates immune responses to myelin antigen in the spleen. The SA–IL-4 fusion protein may be prophylactically and therapeutically advantageous in the treatment of multiple sclerosis.