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Abstract
The development of monoclonal antibodies (mAbs) presents an emerging, highly specific therapeutic strategy for the treatment of multiple sclerosis (MS). mAbs target selective molecules and have shown early promise, along with notable risks, in the treatment of MS and other immune-mediated diseases. The mechanism of action of the 4 mAbs under active investigation for MS (natalizumab, rituximab, alemtuzumab, and daclizumab) are reviewed, with a discussion of how mAb interaction with each target antigen may produce direct and indirect effects (proven and hypothesized) on immune cell activity, CNS-related inflammatory processes, and clinical outcomes.
Glossary
- ADCC=
- Ab-dependent cellular cytotoxicity;
- BBB=
- blood-brain barrier;
- CDC=
- complement-dependent cytotoxicity;
- CEL=
- contrast-enhancing lesion;
- DC=
- dendritic cell;
- FDA=
- Food and Drug Administration;
- IFNβ-1a=
- interferon beta-1a;
- Ig=
- immunoglobulin;
- IL=
- interleukin;
- IL-2R=
- interleukin-2 receptor;
- ITP=
- immune thrombocytopenic purpura;
- mAb=
- monoclonal antibody;
- MoA=
- mechanism of action;
- MS=
- multiple sclerosis;
- NK=
- natural killer;
- PML=
- progressive multifocal leukoencephalopathy;
- RA=
- rheumatoid arthritis;
- RRMS=
- relapsing-remitting multiple sclerosis;
- SC=
- subcutaneous;
- VLA-4=
- very late activating antigen-4.
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