ReviewImmunity, inflammation and disease2026
The Progress of Ferroptosis of Immune Cells in the Tumor Microenvironment and Its Impact on Tumorigenesis and Development.
Review in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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
5 citing papers in PubMed.
- Role of ferroptosis on immunotherapy in breast cancer.Molecular biology reports · 2026Review
- Aflatoxins and Human Health: Global Exposure, Disease Burden, and One Health Strategies.Toxins · 2026Review
- The tumor microenvironment: a dynamic ecosystem and therapeutic nexus in modern oncology.Frontiers in pharmacology · 2026Review
- Beyond angiogenesis: integrating ferroptosis and metabolic rewiring for next-generation RCC therapy.Frontiers in oncology · 2026Review
- The Progress of Ferroptosis of Immune Cells in the Tumor Microenvironment and Its Impact on Tumorigenesis and Development.Immunity, inflammation and disease · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundThe immune cells within the tumor microenvironment (TME) play important roles in tumorigenesis. Ferroptosis is an iron-dependent form of non-apoptotic cell death characterized by the accumulation of lipid peroxides. The interplay between ferroptosis and the tumor immune microenvironment significantly influences the outcome of cancer immunotherapy. The study aims to elucidate the dual effects of ferroptosis on cancer progression and immune responses, particularly in the context of enhancing the efficacy of tumor immunotherapy.
methodsAn extensive literature review was conducted using PubMed to identify studies related to ferroptosis and immune cells in the TME, emphasizing translational research outcomes published within the last 5 years.
resultsThe study reviews the literature on the mechanisms of ferroptosis and its interactions with various components of the TME, including immune cells such as CD8+ T cells, dendritic cells, natural killer cells, regulatory T cells, myeloid-derived suppressor cells, and tumor-associated macrophages. It also examines the impact of ferroptosis inducers and inhibitors on these interactions, alongside the potential synergistic effects of combining ferroptosis induction with current immunotherapies. Ferroptosis plays a dual role in the TME by both promoting and inhibiting tumor growth through its effects on immune cell function. Activation of ferroptosis in tumor cells can enhance the immunogenicity of cancer cells, thereby improving the effectiveness of immunotherapies. Conversely, ferroptosis in immune cells can lead to immune cell dysfunction and contribute to immunotherapy resistance. The study identifies several therapeutic strategies that harness the induction of ferroptosis to overcome resistance to immune checkpoint inhibitors and enhance the anti-tumor immune response. Inducing ferroptosis in tumor cells and immunosuppressive cells, while preventing ferroptosis in effector immune cells, emerges as a promising strategy to enhance the efficacy of immunotherapy.
conclusionThis review highlights the potential of targeting ferroptosis as a sensitization approach to improve cancer treatment outcomes, underscoring the need for further research to fully understand the regulatory mechanisms of ferroptosis in tumor immunity.
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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.