ArticleBlood2009
Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02771197 (Phase II Trial of Lymphodepletion and Anti-PD-1 Blockade to Reduce Relapse in High Risk AML Patients Who Are Not Eligible for Allogeneic Stem Cell Transplantation), which is not on this map. Cited by 83 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.
Phase II Trial of Lymphodepletion and Anti-PD-1 Blockade to Reduce Relapse in High Risk AML Patients Who Are Not Eligible for Allogeneic Stem Cell Transplantation
Who cites it
83 citing papers in PubMed, 148 citations in OpenAlex.
- Phase 2 study of PD-1 blockade following autologous transplantation for patients with AML ineligible for allogeneic transplant.Blood advances · 2023Trial
- Trial
- A phase II study of allogeneic natural killer cell therapy to treat patients with recurrent ovarian and breast cancer.Cytotherapy · 2011Trial
- Mechanisms of T-cell metabolic reprogramming in the microenvironment of acute myeloid leukemia and its therapeutic potential (Review).Oncology letters · 2025Review
- Study on the impact of CD4Clinical and experimental medicine · 2025Article
- Immunosuppressive cells in acute myeloid leukemia: mechanisms and therapeutic target.Frontiers in immunology · 2025Review
- Bone marrow immune cells and drug resistance in acute myeloid leukemia.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- Immunosuppressive microenvironment in acute myeloid leukemia: overview, therapeutic targets and corresponding strategies.Annals of hematology · 2024Review
- Murine Regulatory CD4International journal of molecular sciences · 2024Article
- A novel immunogenic cell death-related classification indicates the immune landscape and predicts clinical outcome and treatment response in acute myeloid leukemia.Cancer cell international · 2024Article
- Recent advances in CAR-T therapy for the treatment of acute myeloid leukemia.Therapeutic advances in hematology · 2024Review
- The graft versus leukemia effect: donor lymphocyte infusions and cellular therapy.Frontiers in immunology · 2024Review
- Influencing factors and solution strategies of chimeric antigen receptor T-cell therapy (CAR-T) cell immunotherapy.Oncology research · 2024Review
- Article
- The Memorial Sloan Kettering Prognostic Score: Correlation with survival in patients with advanced gastric cancer.Cancer medicine · 2023Article
- Acute myeloid leukemia-derived exosomes deliver miR-24-3p to hinder the T-cell immune response through DENN/MADD targeting in the NF-κB signaling pathways.Cell communication and signaling : CCS · 2023Article
- Checkpoint Inhibitors in Acute Myeloid Leukemia.Biomedicines · 2023Review
- The Black Hole: CAR T Cell Therapy in AML.Cancers · 2023Review
- NK cell defects: implication in acute myeloid leukemia.Frontiers in immunology · 2023Review
- The potential role of the thymus in immunotherapies for acute myeloid leukemia.Frontiers in immunology · 2023Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Tumor-induced immune suppression can permit tumor cells to escape host immune resistance. To elucidate host factors contributing to the poor response of adoptively transferred tumor-reactive cytotoxic T lymphocytes (CTLs), we used a systemic model of murine acute myeloid leukemia (AML). AML progression resulted in a progressive regulatory T-cell (Treg) accumulation in disease sites. The adoptive transfer of in vitro-generated, potently lytic anti-AML-reactive CTLs failed to reduce disease burden or extend survival. Compared with non-AML-bearing hosts, transferred CTLs had reduced proliferation in AML sites of metastases. Treg depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced AML disease burden but did not permit long-term survival. In contrast, IL-2DT prevented anti-AML CTL hypoproliferation, increased the number of transferred CTLs at AML disease sites, reduced AML tumor burden, and resulted in long-term survivors that sustained an anti-AML memory response. These data demonstrated that Tregs present at AML disease sites suppress adoptively transferred CTL proliferation, limiting their in vivo expansion, and Treg depletion before CTL transfer can result in therapeutic efficacy in settings of substantial pre-existing tumor burden in which antitumor reactive CTL infusion alone has proven ineffective.
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.