, 2013), sustained recruitment of inflammatory blood-derived macrophages can facilitate extensive secondary axonal dieback and delay the reparative process substantially.
Using a radiation chimera model to distin- guish bone-marrow-derived cells from microglia, Evans and col- leagues determined that the vast majority of accumulated cells in spinal-cord injury are derived from the blood, and Cx3cr1+ mac- rophages but not CCR2+ monocytes are tightly associated with axonal dieback (Evans et al.
Multi-potent adult progenitor cells exhibit similar M(IL-4) polarizing activity, leading to a reduction in macrophage-medi- ated axonal dieback in spinal-cord injury (Busch et al.
Multipotent adult progenitor cells prevent macrophage-mediated axonal dieback and promote regrowth after spinal cord injury.
High-resolution intravital imaging re- veals that blood-derived macrophages but not resident microglia facilitate secondary axonal dieback in traumatic spinal cord injury.
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