Mast cell-deficient mice (W/Wv) 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/Wv 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/Wv mice and wild-type littermates. Mice reconstituted with FcRγ-/- BMMCs or FcγRIII-/- BMMCs exhibited less severe clinical symptoms similar to W/Wv controls, while reconstitution with FcRIIB-/- BMMCs resulted in disease significantly more severe than wild-type controls. Notably, mice reconstituted with FcγRIII-/- 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.
ASJC Scopus subject areas
- Immunology and Allergy