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(American Journal of Pathology. 2007;170:1713-1724.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.060783

Microglial Recruitment, Activation, and Proliferation in Response to Primary Demyelination

Leah T. Remington*, Alicia A. Babcock*{dagger}, Simone P. Zehntner* and Trevor Owens*{dagger}

From the Neuroimmunology Unit,* Montreal Neurological Institute, McGill University, Montreal, Canada; and the Medical Biotechnology Center,{dagger} University of Southern Denmark, Odense, Denmark

We have characterized the cellular response to demyelination/remyelination in the central nervous system using the toxin cuprizone, which causes reproducible demyelination in the corpus callosum. Microglia were distinguished from macrophages by relative CD45 expression (CD45dim) using flow cytometry. Their expansion occurred rapidly and substantially outnumbered infiltrating macrophages and T cells throughout the course of cuprizone treatment. We used bromodeoxyuridine incorporation and bone marrow chimeras to show that both proliferation and immigration from blood accounted for increased microglial numbers. Microglia adopted an activated phenotype during demyelination, up-regulating major histocompatibility class I and B7.2/CD86. A subpopulation of CD45dim-high microglia that expressed reduced levels of CD11b emerged during demyelination. These microglia expressed CD11c and were potent antigen-presenting cells in vitro. T cells were recruited to the demyelinated corpus callosum but did not appear to be activated. Our study highlights the role of microglia as a heterogeneous population of cells in primary demyelination, with the capacity to present antigen, proliferate, and migrate into demyelinated areas.




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