Japanese researchers have identified a chemical that can be used to treat a variety of autoimmune conditions, including rheumatoid arthritis and multiple sclerosis. Some diseases develop when the body’s immune system does not work properly. Instead of attacking bacteria and disease as it should, the immune system attacks healthy cells and tissues.
The effects of autoimmune disorders can be crippling for the millions of people who experience them around the world. Rheumatoid arthritis causes excruciating joint pain, while multiple sclerosis can impair brain and spinal cord function.
“The key to the development of autoimmune diseases, and thus the way to prevent this development, lies in our cells, but the underlying mechanism has always been unclear,” said Professor Hiroki Ishikawa, who heads the Immune Signaling Unit at the Okinawa Institute. of Science and Technology (OIST). “Now our recent research has shed light on a compound that could suppress the development of these diseases.”
Prof. Ishikawa went on to explain that this research, published in Cell Reports, could lead to the development of treatments for autoimmune diseases.
The research focused on helper T cells 17, or Th17 cells. Th17 cells are a type of T cell – a group of cells that make up the main parts of the immune system. These cells, which exist in large numbers in our gut, have evolved to help us fight invading pathogens, but are sometimes overactivated and mistake normal, healthy tissue for pathogens, leading to autoimmunity. The generation of Th17 cells requires glycolysis, a metabolic process in which glucose is broken down and converted into energy to support the cells’ metabolic needs. Glycolysis is necessary for the growth of not only Th17 cells, but also various cells in our body.
“Interestingly, excessive glycolysis appears to suppress the activity of Th17 cells,” said first author Mr. Tsung-Yen Huang, PhD candidate in the Department of Immune Signaling. “So we hypothesized that molecules produced during glycolysis could inhibit cells.”
Enter phosphoenolpyruvate or PEP for short. This chemical compound is a metabolite produced when glucose is converted into energy. Because it is part of such an important process, PEP is generated every day in our bodies. The researchers found that PEP treatment can inhibit the maturation of TH17 cells, leading to resolution of the inflammatory response.
Mr. Huang explained that this was a puzzling result at first because it contradicted all other research on the subject, but he decided to persevere and take a closer look at what might have happened.
The research led them to a protein called JunB, which is essential for the maturation of Th17 cells. JunB promotes Th17 maturation by binding to a set of specific genes. The researchers found that PEP treatment inhibited the generation of Th17 cells by blocking JunB activity.
Armed with this knowledge, the researchers proceeded to treat mice that had autoimmune neuroinflammation with PEP. This disease is very similar to multiple sclerosis and these mice showed positive signs of recovery. The researchers have now filed a patent to continue this research.
“Our results show the clinical potential of PEP,” explained Mr. Huang. “But first we need to increase its efficiency.”
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