ArticleNature cancer2021
LILRB3 supports acute myeloid leukemia development and regulates T-cell antitumor immune responses through the TRAF2-cFLIP-NF-κB signaling axis.
Article in Nature cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 80 citations in OpenAlex.
- Bacterial targeting of the neutrophil inhibitory receptor LILRB3 to evade antibody immunity.Nature communications · 2026Article
- Claudins interact with LILRB immune inhibitory receptors to promote myeloid immunosuppression in cancer.Science immunology · 2026Article
- Tumour necrosis factor receptor-associated factor 7 drives leukaemogenesis through the TWIST1-P2RX1-CaJournal of translational medicine · 2026Article
- Review
- Advances in research on hyperoxia-induced acute lung injury: from pathogenesis to therapy.Frontiers in cell and developmental biology · 2026Review
- The structure and functions of TRAF families and recent advances of TRAFs in leukemia.Frontiers in oncology · 2026Review
- Comprehensive analysis of the leukocyte immunoglobulin-like receptor family in clear cell renal cell carcinoma.Annals of medicine · 2025Article
- Oligomeric cystatin C supports the immunosuppressive activity of myeloid cells through interaction with inhibitory receptors.Signal transduction and targeted therapy · 2025Article
- Molecular and Clinical Insights intoInternational journal of molecular sciences · 2025Review
- Review
- Secretogranin 2 binds LILRB4 resulting in immunosuppression.Nature immunology · 2025Article
- Lymph node transcriptomic profiles suggest susceptibility to bleomycin-induced pulmonary toxicity in classic hodgkin lymphoma.Scientific reports · 2025Article
- PILRα on tumor cells interacts with the T cell surface protein CD99 to suppress antitumor immunity.Nature cancer · 2025Article
- Eph Receptors Activate Myeloid Checkpoint Receptor LILRB5 to Support Tumor Development.Cancer immunology research · 2025Article
- Immunoglobulin-like transcript 5 polarizes M2-like tumor-associated macrophages for immunosuppression in non-small cell lung cancer.International journal of cancer · 2025Article
- LILRB3 genetic variation is associated with kidney transplant failure in African American recipients.Nature medicine · 2025Article
- A Switch Protein Adapter for Anti-LILRB4 CAR-T Cells.European journal of immunology · 2025Article
- TRAF2 regulates the progression of pulmonary fibrosis through β-catenin-Snail signaling pathway.Frontiers in public health · 2025Article
- The role of TRAF2 in pan-cancer revealed by integrating informatics and experimental validation.Frontiers in pharmacology · 2025Article
- Inhibitory leukocyte immunoglobulin-like receptors, subfamily B (LILRBs) in human diseases: structure, roles, mechanisms, and clinical applications.Theranostics · 2025Review
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14 authors at 4 institutions in 2 countries.
Funding
Abstract
Leukocyte immunoglobulin-like receptor B (LILRB), a family of immune checkpoint receptors, contributes to acute myeloid leukemia (AML) development, but the specific mechanisms triggered by activation or inhibition of these immune checkpoints in cancer is largely unknown. Here we demonstrate that the intracellular domain of LILRB3 is constitutively associated with the adaptor protein TRAF2. Activated LILRB3 in AML cells leads to recruitment of cFLIP and subsequent NF-κB upregulation, resulting in enhanced leukemic cell survival and inhibition of T-cell-mediated anti-tumor activity. Hyperactivation of NF-κB induces a negative regulatory feedback loop mediated by A20, which disrupts the interaction of LILRB3 and TRAF2; consequently the SHP-1/2-mediated inhibitory activity of LILRB3 becomes dominant. Finally, we show that blockade of LILRB3 signaling with antagonizing antibodies hampers AML progression. LILRB3 thus exerts context-dependent activating and inhibitory functions, and targeting LILRB3 may become a potential therapeutic strategy for AML treatment.
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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 Socratic graph.