- In autoimmune diseases, T cells mistake healthy parts of the body for pathogens, and attack them
- A study found that if a certain enzyme is not present in T cells, inflammation is substantially decreased
- This discovery can potentially help treat diseases like multiple sclerosis (MS) in humans
An enzyme has been identified as playing a key role in the development of inflammation in autoimmune diseases. Enzymes assist in creating chemical reactions in the body.
The specific enzyme identified by researchers is responsible for the process of breaking down glucose (sugars) in the body and converting it to energy. This process is known as glycolysis.
Researchers associated with the Center for Research on Inflammatory Diseases have found a link between essential organic processes (such as glycolysis) and the immune system.
Researchers conducted a study where they developed experimental autoimmune encephalomyelitis (EAE). EAE is an animal model of brain inflammation, similar to multiple sclerosis (MS) in humans.
The immune system and T cells
T cells form a vital part of the immune system and are responsible for fighting off pathogens. However, with autoimmune diseases such as multiple sclerosis (MS), arthritis, and psoriasis, the T cells mistake healthy parts of the body for pathogens, and attack them.
There are several types of T cells, and T helper (Th) cells are responsible for heightened inflammation in autoimmune diseases.
The researchers found that the enzyme known as pyruvate kinase (PKM2) triggers T cells to attack and cause inflammation, thus worsening symptoms of EAE.
This is done by the enzyme locating the nucleus of the T cell and enhancing its activation.
A further experiment was done using a commercial drug to see what would happen if the PKM22 enzyme could not locate or activate T cells.
Results of the experiment
The study found that firstly, PKM2 plays a role in triggering T cells to develop and maintain inflammation that is brought about by autoimmune disorders, such as MS.
Secondly, it found that when PKM2 is not found in T cells, inflammation is substantially decreased.
The team of researchers confirmed that, “the specific loss of PKM2 in T cells not only significantly reduced the clinical severity but also decreased the incidence of EAE”.
They went on to say, “PKM2, therefore, may represent a potential therapeutic target for autoimmune-mediated inflammation.”
The findings of this study creates the opportunity to improve treatments and the possibility for new treatments for autoimmune diseases.