PLoS Medicine, 2007 · DOI: 10.1371/journal.pmed.0040124 · Published: April 10, 2007
In multiple sclerosis (MS), the body's immune system attacks the protective myelin sheath around nerve fibers, leading to inflammation and nerve damage. Microglial cells, which are immune cells in the brain, can help repair this damage by clearing away cellular debris. This study explores whether modifying myeloid precursor cells (which can turn into microglia) to express TREM2, a receptor that stimulates debris clearance, can improve recovery in an animal model of MS called experimental autoimmune encephalomyelitis (EAE). The findings show that intravenous application of TREM2-transduced bone marrow–derived myeloid precursor cells at the EAE peak led to an amelioration of clinical symptoms, reduction in axonal damage, and prevention of further demyelination.
TREM2 represents a novel therapeutic target for promoting repair and resolving inflammation in MS and other neuroinflammatory diseases.
Myeloid precursor cells can be genetically modified to express TREM2 and used as a cell therapy approach for MS.
Intravenous application of TREM2-transduced myeloid cells could be a feasible method for delivering therapeutic agents to CNS lesions in MS patients.