Over twenty years ago, a research team in the lab of David Hafler, a Yale researcher who was at Harvard at the time, identified a type of T cell in humans that suppresses the immune system. Later, they discovered that these regulatory T cells, when not functioning properly, are a root cause of autoimmune diseases, such as multiple sclerosis (MS). However, the exact mechanism behind this malfunction has remained unclear for many years.

In a recent study led by Yale University, a team of researchers discovered that the loss of immune regulation is caused by an increase in PRDM1-S, a protein involved in immune function. This increase triggers a complex interaction of multiple genetic and environmental factors, such as high salt intake.

The findings, which were published in the journal Science Translational Medicine, also reveal a new target for a universal treatment for human autoimmune diseases.

“These experiments reveal a key underlying mechanism for the loss of immune regulation in MS and likely other autoimmune diseases,” said Hafler, who is also the chair of Yale’s Department of Neurology. “They also provide mechanistic insight into how Treg (regulatory T cells) dysfunction occurs in human autoimmune diseases.”

Autoimmune diseases, common among young adults, are influenced by genetic and environmental factors such as vitamin D deficiency and fatty acids. Sumida and Hafler found that high salt levels contribute to multiple sclerosis development by inducing inflammation in CD4 T cells and causing loss of regulatory T cell function, mediated by a salt-sensitive kinase called SGK-1.e,