The immune signaling molecule interleukin-17A (IL-17A) promotes the recruiting of inflammatory cells to the central nervous system (brain and spinal cord) in a multiple sclerosis (MS) mouse model, a study found.
The findings support the potential of therapies that target IL-17 in MS. IL-17A is part of the IL-17 family of proteins.
The study “Interleukin-17A Serves a Priming Role in Autoimmunity by Recruiting IL-1b-Producing Myeloid Cells that Promote Pathogenic T Cells” was published in the journal Immunity.
Immune cells that produce the signaling IL-17 molecule, called Th17 T-cells, have been identified as key mediators of the inflammatory process in several autoimmune diseases, including psoriasis, rheumatoid arthritis, and MS.
In psoriasis, treatment with antibodies that block IL-17 is highly effective. In an early clinical trial with relapsing-remitting MS (RRMS), treatment with an antibody targeting IL-17 — Cosentyx (secukinumab) — yielded promising results.
However, the exact role of IL-17 in MS is still not clear.
Researchers at Trinity College Dublin investigated the role of IL-17 using a mouse model — experimental autoimmune encephalomyelitis (EAE) — that mimics human MS.
Results showed that EAE mice lacking IL-17 were resistant to MS. While all EAE mice developed severe symptoms 20 days after the triggering of inflammation in the brain and spinal cord (encephalomyelitis), only 35% of EAE mice without IL-17 showed clinical signs of the disease, and these were mild in severity.
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