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  • Updated 07.26.2023
  • Released 08.02.2005
  • Expires For CME 07.26.2026

Natalizumab and PML in MS



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). The author 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.

Key points

• Natalizumab binds to very late activation antigen-4 (VLA-4) on immune cells. These drug-coated cells can no longer bind to CNS endothelium nor cross the blood-brain barrier.

• The drug lowers the number of CSF T cells by at least 10-fold and CSF B cells by 6-fold, and prevents attacks and progression of multiple sclerosis.

• With less immune surveillance in the brain, and perhaps activation of the virus by the treatment, the ordinarily innocuous JC virus can cause progressive multifocal leukoencephalopathy (PML).

• Quantitating serum antibodies to JC virus allows better estimation of risk for progressive multifocal leukoencephalopathy.

• Extending the natalizumab dosing interval from 4 to 6 weeks reduces the risk of PML.

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