. Author manuscript; available in PMC: 2024 Aug 20.

Published in final edited form as: Neurology. 2010 Jan 5;74(Suppl 1):S31–S40. doi: 10.1212/WNL.0b013e3181c97ed3

Table 4.

Mechanisms of action of alemtuzumab^9,48,54,82

Direct effects	Indirect effects	Consequences (therapeutic and side effects)
Depletion of CD52-bearing cells (T and B, NK cells, monocytes and MФ, DCs, some granulocytes)	Stabilization of BBB	Probably most important early therapeutic MoA Decreased CNS immunosurveillance Theoretically immunosuppressive, but only modest rate of infectious complications observed so far
	Repopulation with skewed repertoire: early B-cell repopulation, late T-cell repopulation; CD25^high T cells, Caspase3⁺ T cells	Theoretical benefits for long-term efficacy but may also underlie Ab-mediated autoimmune complications

NK, natural killer cells; MФ, macrophages; DCs, dendritic cells; BBB, blood-brain barrier; MoA, mechanism of action; CNS, central nervous system