Exploring Autoimmune Disease: Finding the Triggers of Immune System Attacks
Posted on December 1, 2017
A study by the University of North Carolina Lineberger Comprehensive Cancer Center may provide new insight into what triggers the development of autoimmune disease.
Over 50 million people in the U.S. live with one or more autoimmune conditions, according to the American Autoimmune Related Diseases Association Inc., a nonprofit organization that focuses on advocacy for people living with autoimmune disease and the advancement of research to find autoimmune cures.
Researchers on the UNC project identified a new trigger in cells of the immune system that may signal the immune system to attack. The trigger prompts the body to increase the production of Th17 cells, a CD4 helper T-cell.
Understanding Why the Immune System Attacks
T-cells are white blood cells that play an important role in the body’s ability to defend itself against disease-causing micro-organisms.
Researchers have long known that Th17 T-cells are pro-inflammatory cells and signal the body to flood areas of infection or injury with additional cells to help fight off illness and infection. But until now they were unsure of what sparked the body to amp up Th17 production.
Although Th17 cells play an essential role in protecting the body against illness, an overproduction of Th17 cells can trigger the development of some cancers and other conditions. High levels of Th17 cells can also contribute to the rejection of organ, tissue and bone marrow transplants.
The study authors identified a series of chemical signals that cause Th17 production.
The signal sequence starts when the interleukin-6 signaling loosens the DNA at the site of the gene that controls Th17 production. Researchers then discovered the next step in the process was the release of Ski-Smad4, a molecular complex that blocks the expression of DNA.
Once the Ski-Smad4 is released, the body starts producing Th17 cells.
The discovery could lead to new treatments or drug therapies that could slow down or block the production of Th17 cells in individuals with autoimmune disease.
Implications of Immune System Attacks
“Limiting the body’s ability to amplify Th17 cell production means a decrease in the painful inflammation that accompanies many autoimmune diseases,” said Dr. Joel Singer, M.D.
Singer is a New York physician who treats patients with autoimmune diseases like lupus, scleroderma, Crohn’s disease and autoimmune hepatitis.
“When the body’s immune system sees healthy tissue as a threat, its natural defense is to attack and kill that tissue. It does this by causing inflammation at the site of the threat,” Singer said.
Autoimmune conditions often attack the joints, muscles and skin, but organs and other body systems are also affected when the immune system malfunctions. Multiple areas and organs are often affected at the same time, which can translate into various diseases.
“Most people with autoimmune diseases have more than one condition, which means increased episodes of pain, fatigue and other life-altering symptoms,” Singer said.
While the UNC research into Th17 cells continues to develop, Singer is treating patients living with autoimmune diseases with adipose fat stem cell therapy.
“Fat stem cells have significant anti-inflammatory properties that reduce inflammation caused by the overproduction of Th17 cells,” Singer said.
Reducing inflammation helps cells return to normal function, which reduces pain and other side effects of many autoimmune diseases.
“Using stem cell therapy is also a way to push the reset button on the immune system. Stem cells are immuno-modulators, so they go in and assess damage and immediately begin to repair the immune system back to normal,” Singer said
Returning the immune system to normal function reduces the occurrence of future attacks on the body so that patients can have more extended periods of remission from their disease.
UNC Lineberger Comprehensive Cancer Center. “Details uncovered in development of immune cell implicated in cancer, autoimmune diseases.” ScienceDaily. ScienceDaily, 26 October 2017.