Trial reportMultiple sclerosis (Houndmills, Basingstoke, England)2014
Daclizumab reduces CD25 levels on T cells through monocyte-mediated trogocytosis.
Trial report in Multiple sclerosis (Houndmills, Basingstoke, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 30 citations in OpenAlex.
- Long-term safety and efficacy of daclizumab beta in relapsing-remitting multiple sclerosis: 6-year results from the SELECTED open-label extension study.Journal of neurology · 2020Trial
- Monocytes and Granulocytes Reduce CD38 Expression Levels on Myeloma Cells in Patients Treated with Daratumumab.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Trial
- Article
- The Biological Significance of Trogocytosis.Results and problems in cell differentiation · 2024Article
- A CD64/FcγRI-mediated mechanism hijacks PD-1 from PD-L1/2 interaction and enhances anti-PD-1 functional recovery of exhausted T cells.Frontiers in immunology · 2023Article
- CD4Frontiers in immunology · 2022Review
- Review
- Extensive Healthy Donor Age/Gender Adjustments and Propensity Score Matching Reveal Physiology of Multiple Sclerosis Through Immunophenotyping.Frontiers in neurology · 2020Article
- Review
- The effects of interleukin-2 on immune response regulation.Mathematical medicine and biology : a journal of the IMA · 2018Article
- Daclizumab.Hospital pharmacy · 2016Article
- Spotlight on daclizumab: its potential in the treatment of multiple sclerosis.Degenerative neurological and neuromuscular disease · 2016Review
- Therapeutic efficacy of monthly subcutaneous injection of daclizumab in relapsing multiple sclerosis.Biologics : targets & therapy · 2016Review
- Daclizumab reverses intrathecal immune cell abnormalities in multiple sclerosis.Annals of clinical and translational neurology · 2015Article
- Induction of interleukin-6 production by rituximab in human B cells.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Possible implication of Fc γ receptor-mediated trogocytosis in susceptibility to systemic autoimmune disease.Clinical & developmental immunology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Daclizumab is a humanized monoclonal antibody that prevents interleukin-2 (IL-2) binding to CD25, blocking IL-2 signaling by cells that require high-affinity IL-2 receptors to mediate IL-2 signaling. The phase 2a CHOICE study evaluating daclizumab as a treatment for multiple sclerosis (MS) included longitudinal analysis of activated T cell counts. Whereas an exposure-dependent relationship was observed between daclizumab and reductions in HLA-DR(+)-activated T cells, a similar relationship was not observed for reductions in CD25 levels. The objective of this report is to determine the mechanism by which daclizumab reduces CD25 levels on peripheral blood mononuclear cells (PBMCs) using cytometric techniques. Daclizumab reduced T cell CD25 levels through a mechanism that required the daclizumab-Fc domain interaction with Fc receptors (FcR) on monocytes, but not on natural killer (NK) cells, and was unrelated to internalization or cell killing. Activated CD4(+) T cells and FoxP3(+) Treg cells showed evidence of trogocytosis of the CD25 antigen in the presence of monocytes. A daclizumab variant that retained affinity for CD25 but lacked FcR binding did not induce trogocytosis and was significantly less potent as an inhibitor of IL-2-induced proliferation of PBMCs. In conclusion, Daclizumab-induced monocyte-mediated trogocytosis of CD25 from T cells appears to be an additional mechanism contributing to daclizumab inhibition of IL-2 signaling.
Indexed as
Identifiers
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.