A cell-signaling molecule is essential for the signaling that leads to neuroinflammation in an animal model of multiple sclerosis, reports two studies published online in Nature Immunology.
Immune cells that attack the central nervous system (CNS) underlie autoimmune diseases such as multiple sclerosis.
Groups led by Burkhard Becher and Abdolmohamad Rostami show activated T cells that are capable of recognizing “self” myelin proteins, found around axons, infiltrate the brain tissue and secrete the cell-signaling molecule GM-CSF in response to another inflammatory mediator called interleukin 23 (IL-23). GM-CSF perpetuates the neuroinflammation process by instructing other immune cells to produce more IL-23. Mice whose T cells cannot produce GM-CSF did not develop neuroinflammation, thus GM-CSF is responsible for disease manifestation in this experimental model.
This scenario suggests feed-forward loop of IL-23 and GM-CSF driving the pathogenic encephalitogenic immune response. Whether GM-CSF drives neuroinflammation in MS remains unknown, but the current findings highlight the potential that IL-23 and GM-CSF might serve a similar role in human disease.