Kieseier, CNS Drugs. 2011 Jun 1;25(6):491-502.
The mechanism of action of IFNβ is complex:
- Increases the expression and concentration of anti-inflammatory agents and downregulates the expression of proinflammatory cytokines (messenger molecules that the cells of the immune system use to communicate with each other).
- Reduces the trafficking of inflammatory cells across the blood-brain-barrier.
- Increases nerve growth factor production, which may lead to an increase in neuronal survival and repair.
- Increases the number of natural killer cells in the peripheral blood; these cells are efficient producers of anti-inflammatory mediators, and may have the ability to curb inflammation.
IFNβ’s actions manifest clinically as reduced MRI lesion activity, reduced brain atrophy, increased time to reach clinically definite MS after the onset of neurological symptoms, decreased relapse rate and reduced risk of sustained disability progression.
“The one action that did not make this list and should have is its effect on viruses, both external viruses for example flu and internal or persistent viral infections such as EBV and other herpes viruses. By reducing reactivation of the viruses that live within our bodies interferon-beta may reduce MS disease activity. This is something we are studying at present in relation to EBV.”