Abstract

Monoclonal antibodies are a promising new class of therapeutic agents that can be employed to target specific molecules of the immune system or any tissue. They are currently being tested in a number of clinical trials in autoimmune diseases such as multiple sclerosis (MS). One of these, the humanized monoclonal anti-CD25 antibody daclizumab (Zenapax), is directed against the interleukin-2 (IL-2) receptor alpha chain (CD25) that is involved in clonal expansion of autoreactive T-cells by binding of its ligand IL- 2. Several years ago daclizumab was approved for the prevention of renal allograft rejection. Following promising observations in uveitis, daclizumab has since been tested in a number of small clinical trials in MS based on the rationale that blocking CD25 would prevent the expansion of autoreactive T-lymphocytes. Safety and efficacy data from the preliminary clinical exploration as well as findings about the mechanism of action of anti-CD25 treatment are reviewed here.