Multiple sclerosis (MS) is considered to be an autoimmune disease leading to 
inflammatory demyelination and axonal damage in the central nervous system 
(CNS). Current treatments involve non-specific immunosuppression and 
immunomodulation. The development of monoclonal antibodies for therapeutic use 
allows targeting of specific immune mechanisms. Natalizumab, a monoclonal 
antibody directed against alpha4beta1 integrin that plays a crucial role in the 
transmigration of immune cells across the blood-brain-barrier, has been licensed 
for relapsing-remitting (RR) MS in 2006. Rituximab, directed against CD20 
expressed on pre B-cells and B-cells has been tested successfully in a phase II 
trial and suggests that several B-cell dependent mechanisms may be relevant to 
the mode of action. Alemtuzumab, targeting CD52 expressed on T-cells, B-cells, 
monocytes and macrophages, has also shown to be effective in early RRMS and 
phase III trials are currently ongoing. Daclizumab binds to CD25, the alpha 
chain of the interleukin (IL)-2 receptor, and is also being tested for RRMS. 
Beside the clinical data the results from these clinical trials give also new 
insights into the pathogenesis of MS. We critically discuss the potential but 
also the pitfalls and potential hazards of these new therapeutic strategies.