Studies Show Certain Protein Could Benefit Multiple Sclerosis
As conventional medicine advances with the goal of slowing the advancement of multiple sclerosis, certain fields of research are turning toward correcting the immune system itself, or finding a way to stop improper communication of immune cells in the body. This field recently made an important discovery by analyzing a signaling protein created by immune b-cells. Proper implementation of the analyzed protein, interleukin-35 (IL-35), may open the door to new therapy options for individuals with multiple sclerosis.
The role of interleukin-35
Scientists discovered IL-35 while examining the ways that immune cells associate and communicate with surrounding cells. They suspected that immune cells only began to attack healthy cells in the body once something went wrong that prevented or interrupted healthy communication. The signaling protein in question, IL-35, is responsible for this communication, and is produced by healthy immune b-cells.
The protein acts as a regulator, telling the b-cell whether or not the cell that is interacting with is a healthy, normal cell, or a foreign, pathogenic enemy invader. If IL-35 fails to indicate to the b-cell that the healthy cell is indeed normal and healthy, the b-cell may be triggered to attack the healthy cell and treat it as a foreign pathogen. The result of these attacks are inflammation and damage to the healthy cells, which at a high enough magnitude can cause large scale system failures or symptoms.
The first applications of the IL-35 protein were in mice models of autoimmune uveitis, a disease identified by inflammation of the inner layers of the eyes. Scientists were able to successfully reduce inflammation of the eyes by introducing IL-35 into the mice populations. Once these anti-inflammatory properties were discovered, researchers immediately began to wonder if the protein had applications to all autoimmune diseases, including multiple sclerosis.
IL-12p35 subunit protein applications
Using IL-35 in practice proved to be more difficult than researchers initially expected. The full protein is complex and difficult to synthetically engineer, and additionally, it is unstable in solution. Though scientists could replicate the protein in a lab, it was clear that there would be no practical applications as a therapy should the research outcomes prove positive. Scientists then decided to test the applications of the protein’s subunits.
IL-35 is made up of two smaller, less unstable compounds called IL-12p35 and Ebi3. These two compounds bind together to form the full protein, and scientists suspected that the anti-inflammatory properties of the full protein could be recreated using only one of the subunits. They tested the mice with autoimmune uveitis again, this time only introducing the IL-12p35 subunit to the mice population.
The effects of the study were excellent. IL-12p35 successfully demonstrated anti-inflammatory effects of a similar magnitude and effectiveness of the full IL-35 protein. Scientists also observed that the subunit of IL-35 protein promoted the growth of b-cells that had a positive, counter effect to negative immune system responses. This not only stopped the symptoms of inflammation in the mice with uveitis, but reversed them altogether.
This exciting discovery marked one of the first times that an autoimmune response was stopped without applying medication or therapy designed to limit or reduce immune cell count in the bloodstream. The discovery was so impactful that senior author of the study, Dr. Charles Egwuagu, Chief of the Molecular Immunology section at the National Eye Institute’s Laboratory of Immunology, said that “these individual subunits may form a new generation of biologics that can be used to treat autoimmune and neurodegenerative diseases.”
Read on to learn more about what this means for multiple sclerosis.