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Monday, August 15, 2016

Tysabri’s Success in Impairing the Immune System in RRMS May Be Source of Its Problems


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Although Tysabri (natalizumab) is a highly effective in treating patients with relapsing-remitting multiple sclerosis (RRMS), some may develop progressive multifocal leukoencephalopathy (PML). According to a new study, this occurs because Tysabri impairs immune surveillance in the central nervous system and reactivates the latent John Cunningham polyomavirus (JCV).
The study, “Natalizumab Affects T-Cell Phenotype in Multiple Sclerosis: Implications for JCV Reactivation,” published in the journal PLOS One, was developed by researchers at Sapienza University in Italy.
Tysabri, an anti-CD49d humanized monoclonal antibody, is known to impair the migration of inflammatory cells into the central nervous system (CNS), leading to a significant decrease in relapses in RRMS patients. It is currently one of the most effective therapies against RRMS, but reactivation of JCV — with consequent development of PML — often limits its use.
Currently, standard of care for RRMS patients includes the routine measurement of anti-JCV antibodies in the serum to assess patients’ risk of developing PML. But some patients have JCV infections even without detectable antibody responses, suggesting that additional markers are required to better risk-stratify patients for PML.
Previous studies have reported that Tysabri modifies the number of certain immune cells in circulation, and decreases CD49d expression at the surface of the immune cells. Therefore, the researchers aimed to assess CD49d expression and alterations in circulating immune cells in a long-term setting that could correlate with JCV reactivation.

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