ArticleNature communications2018
Induction of immunosuppressive functions and NF-κB by FLIP in monocytes.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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Who cites it
36 citing papers in PubMed, 52 citations in OpenAlex.
- c-FLIP as a master regulator of immune homeostasis and disease mechanisms.Cell death & disease · 2026Review
- Regulated cell death in cancer: Mechanisms, crosstalk, and opportunities for therapy.Cancer letters · 2025Review
- Activation of the integrated stress response and loss of cFLIPCell death discovery · 2025Article
- Potential role of CFLAR in enhancing 5-FU sensitivity and modulating immune cell infiltration in breast cancer.European journal of medical research · 2025Article
- The roles of arginases and arginine in immunity.Nature reviews. Immunology · 2025Review
- Cellular collusion: cracking the code of immunosuppression and chemo resistance in PDAC.Frontiers in immunology · 2024Review
- The role of myeloid-derived suppressor cells in liver cancer.Discover oncology · 2023Review
- Targeting tumour-reprogrammed myeloid cells: the new battleground in cancer immunotherapy.Seminars in immunopathology · 2023Review
- "Open Sesame" to the complexity of pattern recognition receptors of myeloid-derived suppressor cells in cancer.Frontiers in immunology · 2023Review
- Article
- CIMT 2021: report on the 18th Annual Meeting of the Association for Cancer Immunotherapy.Human vaccines & immunotherapeutics · 2022Article
- Cancer bio-immunotherapy XVIII annual NIBIT-(Italian network for tumor biotherapy) meeting, October 15-16, 2020.Cancer immunology, immunotherapy : CII · 2022Article
- Salt-inducible kinase 3 protects tumor cells from cytotoxic T-cell attack by promoting TNF-induced NF-κB activation.Journal for immunotherapy of cancer · 2022Article
- The Cellular Tumor Immune Microenvironment of Childhood Solid Cancers: Informing More Effective Immunotherapies.Cancers · 2022Review
- Fatal cytokine release syndrome by an aberrant FLIP/STAT3 axis.Cell death and differentiation · 2022Article
- Targeting Inhibition of Accumulation and Function of Myeloid-Derived Suppressor Cells by Artemisinin via PI3K/AKT, mTOR, and MAPK Pathways Enhances Anti-PD-L1 Immunotherapy in Melanoma and Liver Tumors.Journal of immunology research · 2022Article
- Interrupting the nitrosative stress fuels tumor-specific cytotoxic T lymphocytes in pancreatic cancer.Journal for immunotherapy of cancer · 2022Article
- Breaking the Immune Complexity of the Tumor Microenvironment Using Single-Cell Technologies.Frontiers in genetics · 2022Review
- Coronavirus Infection-Associated Cell Death Signaling and Potential Therapeutic Targets.Molecules (Basel, Switzerland) · 2021Review
- Review
Corrections and comments
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Authors and funding
26 authors at 8 institutions in 3 countries.
Funding
Abstract
Immunosuppression is a hallmark of tumor progression, and treatments that inhibit or deplete monocytic myeloid-derived suppressive cells could promote anti-tumor immunity. c-FLIP is a central regulator of caspase-8-mediated apoptosis and necroptosis. Here we show that low-dose cytotoxic chemotherapy agents cause apoptosis linked to c-FLIP down-regulation selectively in monocytes. Enforced expression of c-FLIP or viral FLIP rescues monocytes from cytotoxicity and concurrently induces potent immunosuppressive activity, in T cell cultures and in vivo models of tumor progression and immunotherapy. FLIP-transduced human blood monocytes can suppress graft versus host disease. Neither expression of FLIP in granulocytes nor expression of other anti-apoptotic genes in monocytes conferred immunosuppression, suggesting that FLIP effects on immunosuppression are specific to monocytic lineage and distinct from death inhibition. Mechanistically, FLIP controls a broad transcriptional program, partially by NF-κB activation. Therefore, modulation of FLIP in monocytes offers a means to elicit or block immunosuppressive myeloid cells.
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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.