The pro-inflammatory signaling protein interleukin (IL)-17A, which is associated with nerve damage in multiple sclerosis (MS), also has an opposing, and crucial, anti-inflammatory role in cells, a study reports.
These findings may explain why therapies that lower IL-17A levels have failed in clinical trials to treat autoimmune diseases like MS.
The study, “The Cytokine IL-17A Limits Th17 Pathogenicity via a Negative Feedback Loop Driven by Autocrine Induction of IL-24,” was published in the journal Immunity.
A key immune cell involved in autoimmune responses is a T-cell subset called Th17. These Th17 cells produce several pro-inflammatory signaling proteins known as cytokines, including IL-17A.
Studies have shown that elevated IL-17A levels are found in active brain lesions in MS patients and, in combination with other pro-inflammatory molecules, cause inflammation and tissue damage.
While therapies that target and reduce IL-17A have been shown to ease symptoms in people with psoriasis, clinical trials of medicines to block IL-17A in autoimmune diseases like MS and uveitis fail to yield consistent results.
“IL-17 is the prototypical inflammatory immune molecule blamed for autoimmunity in the neuro-retina and the brain, but there’s been some controversy about the role it plays,” Rachel Caspi, PhD, the study’s senior author and chief of the Laboratory of Immunology at the National Eye Institute (NEI), said in a press release.
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