WEDNESDAY, Feb. 5, 2020 (HealthDay News) — A new discovery could lead to better treatments for multiple sclerosis (MS) and other autoimmune diseases, such as psoriasis and rheumatoid arthritis, researchers report.
MS occurs when immune cells get into the central nervous system (the brain and spinal cord), causing nerve damage that results in neurological problems. However, the cause is unclear.
Studies in a mouse model of MS — called experimental autoimmune encephalomyelitis (EAE) — have shown that immune T-cells, which secrete an immune molecule called IL-17, damage the myelin sheath surrounding nerves in the central nervous system (CNS).
Drugs that block IL-17 have shown promise in early clinical trials for treatment of relapsing-remitting MS. The drugs have already been licensed for treating psoriasis.
In this new study, researchers at Trinity College Dublin, in Ireland, identified another role that IL-17 plays in EAE, and possibly in MS. However, research in animals doesn’t always pan out in humans.
“A key role of IL-17 is to mobilize and activate an army of disease-causing immune cells in the lymph nodes that then migrate to the CNS to cause the nerve damage,” study co-leader Kingston Mills said in a college news release. He’s a professor of experimental immunology.
Study co-leader Aoife McGinley said the findings suggest that drugs that block IL-17 may not need to cross the blood-brain barrier to effectively treat MS. She’s a postdoctoral fellow in the School of Biochemistry and Immunology.
“So, as well as shedding new light on the importance of IL-17 as a drugs target in [relapsing-remitting] MS, our research highlights the huge potential of drugs that block IL-17 in the treatment of other autoimmune diseases, such as psoriasis and rheumatoid arthritis,” she said in the news release.
The study was published Feb. 4 in the journal Immunity.
MS affects about 2.3 million people worldwide.
More information
The American Academy of Family Physicians has more on multiple sclerosis.
SOURCE: Trinity College Dublin, news release, Feb. 4, 2020
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