This link between food allergies and MS disease activity highlights an important role of the gut.

A new study identifies a protein regulator responsible for inducing the pathogenic properties of Th17 cells, leading to multiple sclerosis. A research team from Osaka University found that the protein Satb1 triggers a shift in immune cells, causing tissue inflammation and autoimmunity. This breakthrough could lead to new treatments targeting the source of inflammation.

Interleukin 17-producing T-helper cells are a recently-identified class of immune cells that play a major role in protection against invading pathogens. Studies have shown that excessive inflammation induced by Th17 cells is actually one of the underlying causes of many inflammatory and autoimmune disorders. But what causes Th17 cells to cross the line from helpful to harmful? To answer this question, the researchers examined genome organizer protein Satb1.

Using a mouse model of MS, the researchers deleted the Satb1 gene in Th17 cells and found that the disease no longer developed in the mice. Key to this mechanism was the lack of expression of a protein called granulocyte-macrophage colony-stimulating factor by the Satb1-defective Th17 cells. GM-CSF is a pathogenic cytokine that causes localized tissue inflammation in MS. Satb1 was also found to enhance the expression of the GM-CSF gene, confirming its role in promoting inflammation.

Satb1 also blocks the expression of a protein specially designed to suppress T-cell inflammatory activity and prevent autoimmune diseases. This protein, programmed cell death protein 1, was more highly expressed in Satb1-deficient Th17 cells compared with normal Th17 cells, indicating that Satb1 normally inhibits protein expression.

Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. However, the researchers said the results suggest that manipulating Satb1 gene expression in Th17 cells could form the basis of novel treatments for various autoimmune diseases caused by Th17 cells. If they can prevent the pathogenic processes of Th17 cells, they may be able to alleviate or even eliminate disease symptoms.

The study was published in Nature Communications.

According to the study’s authors, the discovery could be translated into a viable drug treatment for MS within a few years.

The single-cell analyses used by the researchers are new and can be used for studying individual cells from tissues.

The findings could shed new light on how the disease progresses and help scientists develop treatments.

A new study suggests that ruptures in the cell membrane initiate degeneration of long nerve fibers, resulting influx of calcium ions.

The survey specifically focuses on what methods patients use to cope with the symptom worsening induced by exposure to heat and cold.

The findings may provide a basis for the development of new drugs to treat MS.

A survey has been developed to gain patient input into secondary progressive MS.