It’s a common ingredient.
Autoimmune diseases are linked to dysfunction in regulatory T cells, which are immune cells responsible for suppressing attacks against the body’s own tissues. A recent study published in Science Translational Medicine has identified a common molecular pathway in these cells that is disrupted in individuals with multiple sclerosis and other autoimmune disorders, leading to diminished suppressive function.
The research also highlights that increased dietary salt intake activates this molecular pathway in regulatory T cells, potentially explaining the established connection between high salt consumption and autoimmune diseases. Dr. Tomokazu Sumida, the study’s lead author and a professor at Yale School of Medicine, explained that the study reveals how environmental and genetic factors contribute to the loss of immune regulation in autoimmune diseases like multiple sclerosis (MS). This discovery points to a new potential target for treating such conditions.
Multiple sclerosis, which affects around 2.8 million people globally, is a chronic autoimmune condition where the immune system attacks myelin, the protective sheath covering nerve fibers. This attack leads to nerve damage, inflammation, and muscle weakness. Autoimmune diseases, including MS, are characterized by a malfunction of immune cells, particularly regulatory T cells, which normally help suppress autoimmune responses and prevent damage to healthy tissues.
The study focused on regulatory memory T cells, which are crucial for maintaining immune balance. Researchers compared gene expression in these cells from individuals with multiple sclerosis and healthy controls. They found that the gene PRDM1, which encodes the BLIMP1 protein, was overexpressed in both regulatory and conventional memory T cells in people with MS. This protein is essential for the function of regulatory T cells. Additionally, there was a notable decline in the ID3 gene, which is important for maintaining FOXP3 expression and the suppressive function of these cells. The findings suggest that increased levels of the shorter form of the BLIMP1 protein, PRDM1-S, could contribute to the dysfunction observed in memory regulatory T cells in MS.
Discussion about this post