Mol Immunol 2002 Sep;38(16-18):1373
Brown M, Tanzola M, Robbie-Ryan M.
Department of Pathology, Emory University School of Medicine, WMB 7311, 1639 Pierce Drive, 30322, Atlanta, GA, USA
It is well established that CD4(+) T cells are of central importance in mediating the autoimmune destruction associated with the neurological demyelinating disease Multiple sclerosis (MS) and the rodent model of MS, EAE (experimental allergic encephalomyelitis).
However, other cells also play a critical role in the inflammatory events that lead to the varying degrees of myelin and axonal damage observed in this disease syndrome.
In this review, we present evidence that mast cells, best studied in the context of allergic disease, contribute to EAE disease pathology.
Using mast cell-deficient mice, we demonstrate that mast cells are necessary for the full manifestation of MOG-induced EAE disease and show that cross-linking of Fc receptors is one mechanism of mast cell activation in disease.
In addition, we provide evidence that mast cells exert influences outside the CNS, perhaps through the effects on the generation of the anti-MOG T cell response.