The autoimmune disease lupus, formally known as systemic lupus erythematosus (SLE), is difficult to treat and a major burden to live with.
The random recurrences of pain, inflammation, and fatigue that accompany the illness areA cruel mystery“For unknown reasons, it causes irreparable damage to the kidneys, brain, heart and other organs, affecting 1.5 million people in the United States.”
Immune cells called Helper T cells It is overactive in SLE patients. At last, scientists may have identified a critical root cause of the problem. A rigorous study led by researchers at Northwestern University and Brigham and Women’s Hospital dug into the details and It may be causing other symptoms.
“So far, all the treatments for lupus are blunt instruments: broad-spectrum immunosuppression.” explain Choi Jae-hyuk, an immunologist at Northwestern University.
“By identifying the cause of this disease, we have discovered a potential treatment without the side effects of current treatments.”
The study, conducted by a team of several dozen scientists led by biochemist Calvin Lo at Northwestern University and immunologists Vanessa Sue Wakresh and Ye Kao at Brigham and Women’s Hospital, suggests that lupus patients have an underlying weakened immune system.It’s well balanced.
Blood tests of 19 SLE patients and 19 participants without autoimmune disease showed important differences in the expression of different types of helper T cells.
These important immune cells are responsible for promoting the production of other immune cells that produce antibodies – proteins that typically bind to, label and neutralize foreign substances or pathogens.
To understand the importance of differential T cell expression, imagine a game of tug-of-war where the knot in the middle is a T cell that can potentially take on two different forms. When the knot is pulled in one direction, the T cell will express in a certain way and become a type of helper T cell. When the knot is pulled in the opposite direction, the T cell will express in the opposite way.
People without autoimmune diseases Aryl hydrocarbon receptor (Australia), which Pulling T cells decisively to one side.
This receptor Considered It is “important in regulating innate and adaptive immunity” and has been linked to many autoimmune diseases, including multiple sclerosis, inflammatory bowel disease, and SLE.
In patients with SLE, AHR is not fully activated in T cells. Signaling molecules called type I interferons appear to be pulling T cells away from their typical expression and function.
As a result, excess immune cells promote autoantibodies that attack the body’s own cells, triggering more type I interferon, creating a positive feedback loop.
When the researchers reintroduced the AHR-activating molecule into blood samples taken from lupus patients, immune cell balance was restored.
“We found that activating the AHR pathway with a small molecule activator or limiting pathological excess of interferon in the blood can reduce the number of these disease-causing cells.” To tell Choi.
“If these effects persist, this could be a potential treatment.”
There’s still a long way to go before drugs inspired by these findings prove safe and effective for treating SLE, but given the limited options currently available to patients, the new findings are a hopeful beginning.
“We think the opportunity here is to not broadly suppress the immune system in patients with autoimmune diseases,” Choi says. explain“But it actually reprograms the cells that are causing the disease.”
This study Nature.
