Scientists may have found a way to manipulate T-helper 17 (Th17) cells so as to lower their ability to trigger inflammation, delaying the onset of multiple sclerosis (MS) in a mouse model and slowing its progression without affecting the entire immune system.
Their findings may lead to new treatments with fewer side effects for MS and other Th17-driven autoimmune diseases.
The study, “The nuclear receptor REV-ERBα modulates Th17 cell-mediated autoimmune disease,” was published in the journal Proceedings of the National Academy of Sciences.
Th17 cells are a subtype of pro-inflammatory T-cells that produce interleukin-17 (IL-17), a molecule that, when produced in excess because Th17 cells are overactive, is associated with the development of such autoimmune diseases as MS, rheumatoid arthritis, and psoriasis.
In MS, dysregulated (overactive) Th17 cells play a key role in the destruction of the myelin, the protective layer of nerve cells, that is a hallmark of the disease.
A molecule that regulates the production of IL-17 in Th17 cells, called retinoic acid receptor-related-orphan-receptor-gamma t (RORγt), has caught scientists’ attention before as a potential target for treating autoimmune diseases.
However, RORγt is also involved in critical processes for other T-cells in the immune system. Treatment approaches that act to block its activity have, so far, resulted in changes to T-cell numbers and diversity that damage the system’s ability to defend the body against invading virus and other threats.
Researchers at the Salk Institute found a potential way to suppress RORγt activity, limiting IL-17 production, without harming the rest of the immune system.
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