ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2013
Daclizumab therapy for multiple sclerosis.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 88 citations in OpenAlex.
- Therapeutic protein-drug interaction assessment for daclizumab high-yield process in patients with multiple sclerosis using a cocktail approach.British journal of clinical pharmacology · 2016Trial
- Blockade of the High-Affinity Interleukin-2 Receptors with Daclizumab High-Yield Process: Pharmacokinetic/Pharmacodynamic Analysis of Single- and Multiple-Dose Phase I Trials.Clinical pharmacokinetics · 2016Trial
- Safety, efficacy, and pharmacokinetics/pharmacodynamics of daclizumab (anti-CD25) in patients with adult T-cell leukemia/lymphoma.Clinical immunology (Orlando, Fla.) · 2014Trial
- Effect of daclizumab high-yield process in patients with highly active relapsing-remitting multiple sclerosis.Journal of neurology · 2014Trial
- Integrated bioinformatics analysis of the effects of chronic pain on patients with spinal cord injury.Frontiers in cellular neuroscience · 2025Article
- Interleukin inhibitors and the associated risk of candidiasis.Frontiers in immunology · 2024Review
- Article
- Nucleic Acids as Novel Therapeutic Modalities to Address Multiple Sclerosis Onset and Progression.Cellular and molecular neurobiology · 2022Review
- A Novel CAR Expressing NK Cell Targeting CD25 With the Prospect of Overcoming Immune Escape Mechanism in Cancers.Frontiers in oncology · 2021Article
- Role of Peripheral Immune Cells-Mediated Inflammation on the Process of Neurodegenerative Diseases.Frontiers in immunology · 2020Review
- Article
- Review
- The Potential for Cancer Immunotherapy in Targeting Surgery-Induced Natural Killer Cell Dysfunction.Cancers · 2018Review
- The effects of interleukin-2 on immune response regulation.Mathematical medicine and biology : a journal of the IMA · 2018Article
- Review
- Immunosuppressant Peptide Abu-TGIRIS-Abu-NHBioNanoScience · 2018Article
- Efficacy of Synthetic Peptide Corresponding to the ACTH-Like Sequence of Human Immunoglobulin G1 in Experimental Autoimmune Encephalomyelitis.Frontiers in pharmacology · 2018Article
- The sequence of disease-modifying therapies in relapsing multiple sclerosis: safety and immunologic considerations.Journal of neurology · 2017Review
- Daclizumab: Development, Clinical Trials, and Practical Aspects of Use in Multiple Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Review
- Pharmacodynamic effects of daclizumab in the intrathecal compartment.Annals of clinical and translational neurology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Daclizumab is a humanized monoclonal antibody of IgG1 subtype that binds to the Tac epitope on the interleukin-2 (IL-2) receptor α-chain (CD25), thus, effectively blocking the formation of the high-affinity IL-2 receptor. Because the high-affinity IL-2 receptor signaling promotes expansion of activated T cells in vitro, daclizumab was designed as a therapy that selectively inhibits T-cell activation. Assuming the previous statement, daclizumab received regulatory approval as add-on therapy to standard immunosuppressive regimen for the prevention of acute allograft rejection in renal transplantation. Based on its putative mechanism of action (MOA), daclizumab represented an ideal therapy for T-cell-mediated autoimmune diseases and was subsequently tested in inflammatory uveitis and multiple sclerosis (MS). In both of these diseases, daclizumab therapy significantly inhibited target organ inflammation. Mechanistic studies in MS demonstrated that the MOA of daclizumab is surprisingly broad and that the drug exerts unexpected effects on multiple components of the innate immune system. Specifically, daclizumab dramatically expands and activates immunoregulatory CD56(bright) NK cells, which gain access to the intrathecal compartment in MS and can kill autologous activated T cells. Daclizumab also blocks trans-presentation of IL-2 by mature dendritic cells to primed T cells, resulting in profound inhibition of antigen-specific T cells. Finally, daclizumab modulates the development of innate lymphoid cells. In conclusion, daclizumab therapy, which is currently in phase III testing for inflammatory MS, has a unique MOA that does not limit migration of immune cells into the intrathecal compartment, but rather provides multifactorial immunomodulatory effects with resultant inhibition of MS-related inflammation.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.