Daclizumab was effective in reducing contrast enhancing lesions and improving clinical scores in patients with relapsing and remitting multiple sclerosis with active disease not controlled by interferon therapy. These results provide evidence for long-term efficacy and support further clinical development of daclizumab.

Excitotoxic neuronal death mediated by N‐methyl‐D‐aspartate (NMDA) glutamate receptors can contribute to the extended brain damage that often accompanies trauma or disease. Both the inflammatory cytokine tumor necrosis factor‐α (TNF‐α) and nicotine have been identified as possible neuroprotective agents to NMDA assault. We find that TNF‐α protection of a subpopulation of cultured cortical neurons to chronic NMDA‐mediated excitotoxic death requires both the activation of the p55/TNFRI, but not p75/TNFRII, and the release of endogenous TNF‐α. Nicotine protection to NMDA was mediated through an α‐bungarotoxin‐sensitive receptor. When coapplied, neuroprotection to NMDA by either TNF‐α or nicotine was abolished but could be recovered with α‐bungarotoxin. These results suggest that the cytokine TNF‐α and α‐bungarotoxin‐sensitive nicotinic neurotransmitter receptors confer neuroprotection through potentially antagonistic pathways. © 1998 John Wiley & Sons, Inc. J Neurobiol 35: 29–36, 1998

We examined whether treatment with daclizumab, a humanized monoclonal antibody specific for the interleukin-2 receptor alpha chain, was safe and efficacious in relapsing-remitting and secondary progressive multiple sclerosis patients. Nineteen ambulatory patients with clinically active disease were treated for 5 to 25 months. Seventeen patients were not responding to other immunotherapies. Daclizumab was generally well tolerated. Sustained clinical improvement (10 patients) or stabilization (9 patients) was observed. Daclizumab treatment produced significant reduction in magnetic resonance imaging activity.