ArticleLeukemia & lymphoma2011
Synergistic enhancement of cellular immune responses by the novel Toll receptor 7/8 agonist 3M-007 and interferon-γ: implications for therapy of cutaneous T-cell lymphoma.
Article in Leukemia & lymphoma, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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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.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- The Role of TRL7/8 Agonists in Cancer Therapy, with Special Emphasis on Hematologic Malignancies.Vaccines · 2023Review
- Profile of differentially expressed Toll-like receptor signaling genes in the natural killer cells of patients with Sézary syndrome.Oncotarget · 2017Article
- Toll-like receptor agonists partially restore the production of pro-inflammatory cytokines and type I interferon in Sézary syndrome.Oncotarget · 2016Article
- Article
- IL-15 and IL-17F are differentially regulated and expressed in mycosis fungoides (MF).Cell cycle (Georgetown, Tex.) · 2014Article
- Gardiquimod: a Toll-like receptor-7 agonist that inhibits HIV type 1 infection of human macrophages and activated T cells.AIDS research and human retroviruses · 2013Article
- The histone deacetylase inhibitor, romidepsin, suppresses cellular immune functions of cutaneous T-cell lymphoma patients.American journal of hematology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Cutaneous T-cell lymphoma (CTCL) is responsive at all stages to immunotherapy. We determined whether a novel agonist for Toll-like receptor (TLR) 7/8 (3M-007) combined with either interferon-γ (IFN-γ) or interleukin-15 (IL-15) would enhance patients' immune responses in vitro. Our data demonstrate that IFN-γ or IL-15 in combination with 007 significantly increases patients' natural killer (NK) cytolytic activity against CTCL tumor cell lines and synergistically induces dendritic cell cytokines, compared to 007 alone. Microarray studies of gene expression of patients' peripheral blood mononuclear cells (PBMCs) primed with IFN-γ followed by stimulation with 007 identified significant up-regulation of the expression of IL-12 p35 (α-chain), IL-12 p40 (β-chain), and nine IFN-α genes. Importantly, the underlying mechanism of increased levels of IFN-α and IL-12 from combined treatment appears to involve IFN regulatory factor 8 (IRF-8). These results further support our hypothesis that combinations of biological modifiers activating different arms of the immune system may provide significant therapeutic benefits for patients with advanced CTCL.
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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.