Immunizing mouse models with Qa-1 derived from myelin prevented multiple sclerosis disease progression.
Findings from a recent animal study suggest that immunizing patients with multiple sclerosis could be an effective way to prevent demyelination. Currently, multiple sclerosis treatments have broad effects on immune cells that come with a broad range of side effects.
Characteristics of this inflammatory disease include demyelination of axons of the central nervous system that results in episodes of transient neurologic deficits. The cause of the disease is unknown, but it is thought to involve both genetic and environmental causes.
The resulting demyelination of the nerves, along with some axonal injury, causes a variety of mental and physical changes.
The immunizations would contain molecules derived from myelin, and these molecules could stop the disease in mouse models of multiple sclerosis. The targeted treatment would prevent adverse effects on immune processes, which could make patients susceptible to infections.
Antigen-specific therapy would target hazardous autoimmune cells that react with myelin, and turn into myelin-specific regulatory T cells, according to a study published by Scientific Reports. These regulatory T cells would instead work to stop an attack on myelin, and would not diminish other immune functions.
Other research found that the molecule Qa-1 may be able to achieve this goal since it is an epitope, which means that it is the segment of an antigen protein that antibodies bind to. Mouse models of multiple sclerosis have autoimmune cells that carry the epitopes, which also alert the immune system to destroy myelin, according to the study.
The molecules can also be used to activate Qa-1 specific regulatory T cells. The scientists found that Qa-1 molecules from autoimmune cells that attack myelin can be used successfully in a vaccine in mouse models.
These vaccines increase the activation of regulatory T cells, and stop the disease process.
If this method is used to treat patients, the scientists need to know which cells attack myelin in order to find the correct epitopes. However, this is difficult to determine in humans, so the scientists chose a different method.
They decided to isolate the epitopes from a protein inside the myelin instead of the immune cells. In mouse models of multiple sclerosis, the scientists searched for Qa-1 epitopes in the myelin protein MOG.
Scientists discovered the desired epitope, and found that it activated regulatory T cells that worked to prevent attacks on cells with Qa-1 epitopes, according to the study. Then, mouse models of multiple sclerosis were immunized with the molecule.
Mouse models immunized with the Qa-1 molecule had an increased number of regulatory cells in the brain, and also had slower disease progression. To determine if the regulatory T cells elicited from the immunization, the scientists transplanted the cells from an immunized mouse model to 1 that was not immunized.
They discovered that mice who received the transplanted regulatory T cells had decreased disease progression. These findings suggest that immunizing patients with human homologues of Qa-1 epitopes could potentially provide a beneficial treatment to patients with multiple sclerosis, the study concluded.