J Immunol 2003 Feb 15;170(4):1630-4
Robbie-Ryan M, Tanzola MB, Secor VH, Brown MA.
Graduate Program in Immunology and Molecular Pathogenesis and Department
of Pathology, Emory University School of Medicine, Atlanta, GA 30322.
Mast cell-deficient mice (W/W(v)) exhibit significantly reduced severity of experimental allergic encephalomyelitis (EAE), a murine model of multiple sclerosis.
In this study, the contribution of FcR-mediated mast cell activation to disease was examined.
W/W(v) mice were reconstituted i.v. with bone marrow-derived mast cells (BMMCs) from wild-type mice or those lacking functional FcRs.
Eight weeks later, EAE was induced by immunization with the myelin oligodendrocyte glycoprotein 35-55 peptide.
Disease scores were analyzed in reconstituted mice and compared with age-matched W/W(v) mice and wild-type littermates.
Mice reconstituted with FcRgamma(-/-) BMMCs or FcgammaRIII(-/-) BMMCs exhibited less severe clinical symptoms similar to W/W(v) controls, while reconstitution with FcRIIB(-/-) BMMCs resulted in disease significantly more severe than wild-type controls.
Notably, mice reconstituted with FcgammaRIII(-/-) BMMC exhibit a relapsing-remitting course of disease.
These data demonstrate that both activating and inhibitory FcRs expressed on mast cells influence the course of EAE.