IGF-1 Could Suppress Immune System in Multiple Sclerosis, Other Autoimmune Disease
Among autoimmune diseases, Multiple Sclerosis is one of the most progressive and debilitating, affecting between 300,000 and 400,000 people in the United States alone. The cause of the disease remains elusive to researchers, making it extremely difficult to research and develop effective therapies for treating symptoms and reversing neural damage. However, it is known that in Multiple Sclerosis, the patient’s own body attacks and degrades the myelin sheath around nerve fibers. Now, a new study entitled “Insulin-like growth factor-1 stimulates regulatory T cells and suppresses autoimmune disease” reports the beneficial effects of a systemic delivery of insulin-like growth factor-1 (IGF-1) in suppressing autoimmune diseases. This new finding suggests a novel approach for toning down the immune system so that in a disease like MS, destruction of myelin can be slowed down or even halted. The results were published on October 22nd issue of EMBO Molecular Medicine.
In autoimmune diseases, the immune system, crucial to defending against harmful pathogens, becomes hyper-reactive and attacks the body’s own cells. In autoimmune patients, a specific group of immune system cells known as pro-inflammatory T-effector cells recognizes the body’s cells as foreign, thus triggering immune responses against it. Additionally, in these disorders, the body’s surveillance system, which is mediated by another class of cells called T-regulatory cells (T-reg) that shut down the immune response triggered by T-effector cells once their work has finished, also fails. As a result, these systemic failures lead to a hyper-activation of the immune system against itself.
Using two mouse models for two autoimmune diseases, type 1 diabetes (STZ and NOD) and multiple sclerosis (EAE), the researchers discovered that systemic delivery of IGF-1 suppressed autoimmune disease progression. Their studies identified that IGF-1 administration led to increased levels of T-reg cells in affected tissues, and these cells maintained their suppressive properties. IGF-1 acts directly on T-reg cells’ population, since removing the IGF-1 receptor, specifically in this cell population, was sufficient to abrogate IGF-1 effects.
Professor Rosenthal, the study’s lead author at the European Molecular Biology Laboratory (EMBL) in Italy, commented, “IGF-1 is already an approved therapeutic and has been tested in many different settings. That means it will be much easier to start clinical trials for IGF-1 in auto-immune and inflammatory diseases than it would if we were proposing a new, untested drug.”
Future research by the team will further explore the role of IGF-1 in other conditions, such as muscular atrophy, fibrosis, and heart disease.