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Bone Marrow-Derived Mast Cells Accumulate in the Central Nervous System During Inflammation but Are Dispensable for Experimental Autoimmune Encephalomyelitis Pathogenesis¹

Jami L. Bennett^2,*, Marie-Renée Blanchet^2,*, Linlin Zhao, Lori Zbytnuik^*,, Frann Antignano, Matthew Gold^*, Paul Kubes and Kelly M. McNagny^3,*,

^* The Biomedical Research Centre, University of British Columbia, Vancouver, British Columbia, Canada; Immunology Research Group, Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada; and British Columbia Cancer Centre, University of British Columbia, British Columbia, Canada

Reports showing that W/W^v mice are protected from experimental autoimmune encephalomyelitis (EAE, a murine model of multiple sclerosis), have implicated mast cells as an essential component in disease susceptibility, but the role of mast cell trafficking has not been addressed. In this study, we have used both mast cell transplantation and genetic mutations (Cd34^–/–, W/W^v, W^sh/W^sh) to investigate the role of mast cell trafficking in EAE in detail. We show, for the first time, that bone marrow-derived mast cells are actively recruited to the CNS during EAE. Unexpectedly, however, we found that EAE develops unabated in two independent genetic backgrounds in the complete absence of mast cells or bone marrow-derived mast cell reconstitution. We conclude that although mast cells do accumulate in the brain and CNS during demyelinating disease via peripheral mast cell trafficking, they are completely dispensable for development of disease.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by the Canadian Institutes of Health Research (CIHR), AllerGen Network Centre of Excellence (to K.M.M.), Multiple Sclerosis Society of Canada (to J.L.B.), Michael Smith Foundation for Health Research (to K.M.M. and M.R.B.), and Fonds de la Recherche en Sante (to M.R.B.).

² J.L.B. and M.R.B. contributed equally to this work.

³ Address correspondence and reprint requests to Dr. Kelly M. McNagny, The Biomedical Research Centre, University of British Columbia, 2222 Health Sciences Mall, Vancouver, British Columbia, Canada. E-mail address: kelly{at}brc.ubc.ca

⁴ Abbreviations used in this paper: WT, wild type; EAE, experimental autoimmune encephalomyelitis; BMMC, bone marrow-derived mast cell; PFA, paraformaldehyde; CAE, chloroacetate esterase; MOG, myelin oligodendrocyte glycoprotein.