How This Protein Can Inhibit Multiple Sclerosis Inflammation

Autoimmune disorders are among the most prevalent chronic, lifelong illnesses that afflict people across the globe today. They are often unpredictable and unique to the individual in their progression, as the diseases associated with autoimmune dysfunction are characterized by a person’s own immune system attacking healthy cells in the body. The cause of this dysfunction is still unknown, and many live with progressive autoimmune disorders waiting for a cure or solution.

Multiple sclerosis is one such autoimmune disease. As of yet, there is no cure to multiple sclerosis, although more and more treatment options are being made available through research and clinical studies of the disease.

As conventional medicine advances with the goal of slowing the advancement of the disease, 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 ways that immune cells associate with 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 it's 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.

Read on to learn about the results of this study, and how the findings can be implemented in future multiple sclerosis research initiatives.