Myeloid Component in Multiple Sclerosis Relapse
A recent paper from the University of Rochester (King et al. Circulating Ly-6C+ myeloid precursors migrate to the CNS and play a pathogenic role during autoimmune demyelinating disease. Blood 2009 Apr 2;113(14):3190-7) reports a novel mechanism by which the immune system may contribute to demyelination in the animal model of multiple sclerosis, experimental allergic encephalomyelitis (EAE).
The investigators observed that before relapses in the EAE model, a flux of myeloid progenitors enter the bloodstream, cross the blood brain barrier, and differentiate into macrophages and dendritic cells, which are believed to play an important role in immune mediated damage to the CNS. Dendritic cells are known to be the most potent activators of T cells, whereas macrophages secrete various inflammatory mediators that contribute to demyelination.
It was found that the factor causing attraction of these myeloid progenitors was GM-CSF, since neutralization of this protein led to decreased myeloid recruitment and less disease severity.
This study suggests, at least in the animal model, that multiple sclerosis is not associated only with T cell activation, but that other cellular components are involved. It is still unclear what causes the initial production of GM-CSF in the brain
Tags: dendritic cell, inflammation, macrophage, multiple sclerosis, myeloid
June 8th, 2009 at 9:21 pm
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