Treatment May Prevent Development of Multiple Sclerosis

Blocking production of specific immune cell protects against onset of MS.

Blocking the production of a particular immune cell may prevent the onset of multiple sclerosis, a recent study indicates.

Using a drug that blocks an immune cell associated with inflammation and autoimmunity, researchers were able to protect against the onset of the disease in mice.

"We are very excited about these findings," co-senior author Eric Verdin, MD, said in a press release. "In light of the significant effect the treatment had on inflammation, the implications of these results will likely extend beyond multiple sclerosis to other types of autoimmune disorders. We are particularly interested in testing this in type I diabetes given the similar pathways involved, and we are already seeing very promising results in preliminary experiments."

In the immune system, Th17 cells activate the immune system to protect against infections and cancers, while regulatory T-cells called Tregs suppress the system. The immune system becomes hyperactive when a disparity occurs between the 2 T-cell types, with too many Th17 cells and not enough Tregs. This disparity can cause inflammation, tissue damage, and autoimmune disease.

For the study, published in the Journal of Experimental Medicine, researchers evaluated the effect of blocking the regulatory protein sirtuin 1 (SIRT1), which is involved in the Th17 cell production. Blocking the protein was found to protect against the onset of autoimmunity.

SIRT1 can also have a negative impact on Treg maturation and maintenance, therefore inhibiting expression of the protein simultaneously increased Tregs production while suppressing Th17 creation.

For the study, the researchers tested a drug in mice that inhibits SIRT1. In a mouse model of MS, the mice typically experience severe motor problems that eventually lead to paralysis.

After receiving treatment, however, not only did the mice behave normally, but they also showed no signs of inflammation or cell damage in their spine.

"The conventional theory has been that you should activate SIRT1 to improve health and longevity, but we show that this can have negative consequences," first author Hyungwook Lim, PhD, said in a press release. "Instead, we think the role of SIRT1 very much depends on the type of tissue being targeted. For instance, in immune cells, instead of being anti-inflammatory SIRT1 appears to have a pro-inflammatory role, which makes it a prime target to treat autoimmune disorders."