According to Myasthenia Gravis News, researchers recently determined a new therapeutic target for myasthenia gravis (MG): activating a bile acid receptor called TGR5. By activating this bile acid receptor, researchers managed to reduce immune response and lower the amount of pro-inflammatory cytokines. As a result, researchers believe it would prevent the body from attacking itself, reducing MG symptoms. Check out the full findings published in Journal of Neuroimmunology.

TGR5

According to ScienceDirect:

Bile acids are a group of chemically similar molecules that have diverse physical and biologic properties. They facilitate the emulsion and absorption of dietary fats and lipid-soluble vitamins.

Basically, bile acids help dissolve and absorb dietary fat. However, some research suggests that bile acids interact with and signal immune cell receptors like TGR5 and FXR-alpha. Both of these receptors have previously been associated with inflammation and immunosuppression.

So researchers questioned whether levels of FXR-alpha and TGR5 were changed in patients with myasthenia gravis. Additionally, researchers measured how activating these receptors changed the way regulatory T-cells and regulatory B-cells (which usually help inhibit overactive immune responses) acted.

First, researchers sourced blood samples from 19 patients with MG. Patient ages ranged from 18 to 79. 42% of patients were male and 58% were female. Additionally, researchers sourced blood samples from 17 controls as well.

Patients with MG had higher TGR5 and FXR-alpha receptors in a type of white blood cell called a monocyte. When treated with a TGR5 agonist called BAR-501, researchers saw lower T-cell counts, particularly those which secreted IFN-gamma and TNF-alpha. But why is this important, you might ask? Well, both of these secretions play a role in inflammation in autoimmune conditions. However, treatment with an FXR-alpha activator showed no significant results.

Patients with MG also had higher levels of interleukin-6 (IL-6), a pro-inflammatory cytokine. Again, BAR-501 reduced IL-6 in patients with MG.

Ultimately, researchers determined that TGR5 seemed to respond well to treatment options. As a result, it shows promise as a therapeutic target in the future.

Myasthenia Gravis (MG)

The aptly named myasthenia gravis, which means “grave muscle weakness,” is an autoimmune neuromuscular disorder in which the body mistakenly attacks itself. Unlike going after germs, viruses, or other foreign invaders, antibodies attack proteins that help the nerves and muscles communicate. As a result, patients with MG experience muscle weakness in voluntarily controlled muscle groups. There is only one form of inherited MG, called congenital myasthenia gravis. Unlike the autoimmune form, gene mutations in congenital MG cause protein malfunction. Generally, activity worsens MG symptoms. However, most patients with MG will not experience life-threatening complications, such as chest wall weakness and breathing failure. Altogether, MG is believed to affect 20 out of 100,000 people across the world.

Patients with congenital MG experience symptom onset in infancy, with the condition lasting throughout life. Transient neonatal MG also begins in infancy, but ends a few weeks later. Finally, juvenile MG often occurs in adolescence. Patients with the latter condition may experience symptomatic periods as well as periods of remission. Symptoms include:

• Eyelid drooping
• Changes in gait
• Slurring speech
• Double vision
• Difficulty with chewing or swallowing
• Muscle weakness in the neck and limbs

Learn more about MG.