Unlocking a key messenger protein in the body’s defences could be a first step to new treatments for multiple sclerosis (MS) and other autoimmune diseases, suggest studies in mice with a form of the disease.
The messenger protein is called granulocyte-macrophage colony-stimulating factor, or GM-CSF for short. The body’s immune of defence system comprises cells, processes and molecules that detect and respond to foreign agents, pathogens and injury to prevent harm and restore health, but in autoimmune diseases these attack healthy tissue instead. The study focussed on a group of immune system cells called T helper 17 cells (Th17), which normally protect cells against invasion by pathogens, but are also known to be involved in autoimmune diseases in humans and animals. The researchers wanted to find out how these cells work.
The researchers showed that GM-CSF could be a key culprit in the onset of MS, because without it, Th17 cells did not induce MS-like disease in mice with autoimmune encephalomyelitis (EAE), commonly used to study the biology of MS. This study revealed a pathway linking GM-CSF signalling and Th17 cells which turns out to be the main route to inflammation in the nervous system in autoimmune diseases like MS.
In earlier research, the same team discovered a related mechanism in MS where another signalling molecule, interleukin-27 (IL-27), helped block the onset of symptoms in animals with an MS-like disease. Bringing the results of the two papers together, they suggest increasing levels of GM-CSF may cause MS, but increasing IL-27 may help quell an overactive immune system.If similar results are found in human blood samples, it may be possible to start looking for a new treatment for multiple sclerosis.
Read more about multiple sclerosis on AnimalResearch.info
Last edited: 6 April 2022 14:07