Tumors and the cells implicated in autoimmune diseases "both express the same inhibitors of cell destruction."
Researchers from George Washington University in Washington, DC, and the Roswell Park Cancer Institute in Buffalo, NY, have found that tumors and the cells implicated in autoimmune diseases both express the same inhibitors of cell destruction.
Survivin, an inhibitor of cell destruction - or "apoptosis" - in tumors, is also expressed in the lymphocytes (white blood cells) of humans and animals with an autoimmune disease called myasthenia gravis.
"We found that humans with myasthenia gravis also express survivin in autoreactive lymphocytes," says Linda Kusner, PhD, assistant research professor in the Department of Pharmacology and Physiology at George Washington. "We found these cells to be part of the dysfunction underlying the autoimmune disease."
A severe muscle disease affecting about 20 out of 100,000 people, patients with myasthenia gravis can become so weak that they require machines to assist their breathing.
There is no known cure for the disease, which is currently managed through a combination of lifestyle changes and medications to improve the communication between the nerves and muscles or to suppress the immune system response.
Symptoms of myasthenia gravis 'reversed by eliminating survivin-expressing cells'
Although Medical News Today did not have access to the study at the time of publication, in a news release the team claims that by using a vaccine technique where they eliminated cells expressing survivin, they were able to improve symptoms of myasthenia gravis in an animal model.
Fast facts on myasthenia gravis
- In people with myasthenia gravis, the body produces antibodies that block the muscle cells from receiving messages from the nerve cells
- The muscle weakness causes difficulties with breathing, chewing, swallowing, climbing stairs, lifting objects, standing up, talking and maintaining a steady gaze
- Patients may also experience facial paralysis, fatigue, changes to their voice, double vision and drooping eyelids.
The next step for the team is to investigate how this technique might be applied to human patients.
Dr. Henry Kaminski, chair of the Department of Neurology at the George Washington School of Medicine and Health Sciences, says:
"This study opens a new therapeutic approach for myasthenia gravis, as well as other autoimmune disorders. Conventional therapies may improve the disease but have numerous complications."
"This discovery may lead to a viable treatment option for the millions of American suffering from these disorders," he adds.
In 2013, research from Georgia Regents University in Augusta suggested that an antibody to LRP4 - a protein that is important in enabling the brain to communicate with muscles - is a cause of myasthenia gravis.
The team behind that study administered LRP4 antibodies to healthy mice, who then displayed "classic symptoms" of myasthenia gravis. The mice also experienced degradation of the neuromuscular junction - the point where the brain and muscle talk.