The immune system coming ready for battle against bacteria, viruses, fungi and even cancer. But in cases of autoimmune disease; the immune system cells superpowers turn it into a supervillain. But now scientists have discovering a way to stop certain immune system cells from mistakenly attacking the body. Suggesting that a new way to target Th17 helper T cells; a type of immune cell that produces interleukin 17, a molecule known to be at the root of autoimmune diseases such as multiple sclerosis; rheumatoid arthritis and psoriasis.
In an autoimmune disease situation, the immune system turns its weapons on itself; Autoimmune diseases affect around 1 in 30 people. This research opens the door to treating these patients without triggering harmful side effects. By using a mouse model of multiple sclerosis to investigate the overproduction of interleukin 17 in Th17 helper T cells.
These immune cells normally work to cure infections; with interleukin 17 sending an inflammation signal to help kick off the immune response. However, sometimes the immune cells become hyperactive and start churning out too much interleukin 17, damaging nearby tissues and kicking off the autoimmune disease process. Drug treatments can slow interleukin 17 production; but they also work as powerful immuno suppressants; blocking the body’s overall ability to fight infections.
Immune system cells
The team uncovered a way to use a molecule called REV-ERB to suppress interleukin 17 production. REV-ERB binds to a site on the Th17 helper T cells that is normally occupied by a molecule called ROR, responsible for interleukin 17 production. By taking over the same binding location, REV-ERB competes with ROR. “ROR is a gas pedal that drives these helper T cells, but REV-ERB is like the brakes.
The researchers then showed they were able to chemically activate REV-ERB and delay the onset and slow the progression of symptoms of experimental autoimmune encephalomyelitis; the mouse model of multiple sclerosis. More work is needing, but the scientists say targeting this particular pathway offering a way to tamp down; interleukin 17 expression without affecting the rest of the immune system.
Treatment with a synthetic REV-ERB agonist delays the onset and impedes the progression of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Taking together, our study suggesting that modulating REV-ERBα activity may be using to manipulate Th17 cells in autoimmune diseases.
It’s an early stage, but it’s certainly encouraging; Th17 cells are a subset of T cells that produce the interleukin 17 and other proinflammatory cytokines. They are involving in the development of autoimmune diseases such as multiple sclerosis and rheumatoid arthritis.