White blood cells use adhesion molecules to attach to CNS endothelial cells, then penetrate the blood-brain barrier, and then cause inflammatory demyelination in multiple sclerosis. Antibodies to the VLA-4 adhesion molecule (natalizumab) prevent exacerbations and progression of multiple sclerosis. Some patients on this therapy have developed progressive multifocal leukoencephalopathy (PML).
In this article, Dr. Anthony Reder of the University of Chicago discusses the role of adhesion molecules in immune activation, penetration of the blood-brain barrier, and provocation and prevention of PML. The most recent information on monitoring for PML and clear definitions of the risk of PML are detailed.
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