Hope for new motor neuron disease therapy

Interleukin-2 is a potential treatment for amyotrophic lateral sclerosis, or ALS, also known as motor neuron disease, French researchers have reported.

A team led by Professor William Camu of the University Hospital of Montpellier, France, explain that neuroinflammation is a feature of ALS. So they investigated the effectiveness of giving low-dose interleukin-2, which has previously been found to enhance regulatory T-cell function in other auto-inflammatory conditions.

Circulating regulatory T cell lymphocytes also contribute to the inflammatory response in ALS, and their action depends on interleukin-2 for their survival.

For the study, 36 ALS patients at centres in the UK and France were given the standard treatment, riluzole, for three months. Then a third were given placebo, and the other two-thirds were given interleukin-2 at one of two dose levels.

Treatment was given by injection over five days every month for three months. All patients were followed for 18 months to monitor safety, disease biomarkers and symptoms.

This showed that interleukin-2 was safe and well-tolerated, and increased regulatory T cell numbers in the blood. Furthermore, it improved the function of these regulatory T cells.

Details appeared yesterday (7 July) in EBioMedicine. The authors report: “Changes in blood cytokines and chemokines were in keeping with the notion that linterleukin-2 reduces the harmful effects and enhances the beneficial effects of immune activity in the nervous system in ALS.

“Overall, these findings strongly support further investigation of interleukin-2 in ALS and provide crucial insights on which to base larger trials designed to detect improvement in day to day activity and survival in ALS.”

Camu, W. et al. Repeated 5-day cycles of low dose aldesleukin in amyotrophic lateral sclerosis (IMODALS): A phase 2a randomised, double-blind, placebo-controlled trial. EBioMedicine 7 July 2020 doi: 10.1016/j.ebiom.2020.102844

https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(20)30219-X/fulltext

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