Harald Neumann and colleagues from the University of Bonn modified myeloid precursor cells to express a protein (triggering receptor expressed on myeloid cells-2 (TREM2), which is normally made by microglia - a cell from the nervous system - and injected these TREM2-expressing cells into the veins of mice with experimental autoimmune encephalomyelitis (EAE, an animal model of MS).
The researchers examined the migration of these cells into the spinal cord of the mice, their effect on the symptoms of EAE, and what effect there was on the clearance of cell debris and inflammatory responses in the spinal cord of the mice. They found that neither TREM2-expressing nor control myeloid precursor cells migrated into the spinal cord when injected into healthy mice or into animals just beginning to show the symptoms of EAE. However, both control and modified cells migrated into the spinal cord when injected into animals when EAE symptoms were at their peak. The injection of TREM2-expressing myeloid precursor cells (but not control myeloid precursor cells) at this time reduced EAE symptoms and nerve damage, and halted loss of myelin and also increased the clearance of cell debris and myelin fragments.
These findings will need to be repeated in further animal models before the implications for human disease are clear; however, they open up an avenue of further research.
Citation: Takahashi K, Prinz M, Stagi M, Chechneva O, Neumann H (2007) TREM2-transduced myeloid precursors mediate nervous tissue debris clearance and facilitate recovery in an animal model of multiple sclerosis. PLoS Med 4(4): e124.
Andrew Hyde | alfa
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