ArticleNature cell biology2015
The ITIM-containing receptor LAIR1 is essential for acute myeloid leukaemia development.
Article in Nature cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
What it found
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Who cites it
89 citing papers in PubMed, 137 citations in OpenAlex.
- LAIR1 suppresses phagocytosis via SHP2/USP22-mediated MYH9 degradation in glioma-associated microglia/macrophages to drive immunosuppression.British journal of cancer · 2026Article
- Article
- LAIR1 prevents excess inflammatory tissue damage in Staphylococcus aureus skin infection and Cutaneous T-cell Lymphoma.JCI insight · 2025Article
- Intraepithelial Lymphocytes and LAIR1 Expression in Celiac Disease.Biomedicines · 2025Article
- Inhibitory pattern recognition receptors: lessons from LAIR1.Nature reviews. Immunology · 2025Review
- NC410, a bivalent LAIR-2 construct, remodels collagen in the tumor microenvironment and abrogates neutrophil-driven T cell suppression.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Targeting LAIR1-mediated immunosuppression adds a new weapon to our immunotherapy arsenal.The Journal of clinical investigation · 2025Article
- LILRB1 enhances the progression of diffuse large B-cell lymphoma through the CREB-SORBS3 pathway.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Cholesterol metabolism regulated by CAMKK2-CREB signaling promotes castration-resistant prostate cancer.Cell reports · 2025Article
- The Role of LAIR1 as a Regulatory Receptor of Antitumor Immune Cell Responses and Tumor Cell Growth and Expansion.Biomolecules · 2025Review
- Eph Receptors Activate Myeloid Checkpoint Receptor LILRB5 to Support Tumor Development.Cancer immunology research · 2025Article
- Review
- A Switch Protein Adapter for Anti-LILRB4 CAR-T Cells.European journal of immunology · 2025Article
- Is modulation of immune checkpoints on glioblastoma-infiltrating myeloid cells a viable therapeutic strategy?Neuro-oncology · 2025Review
- Polymorphisms in immunosuppression-related genes are associated with AML.Frontiers in immunology · 2025Article
- Inhibitory leukocyte immunoglobulin-like receptors, subfamily B (LILRBs) in human diseases: structure, roles, mechanisms, and clinical applications.Theranostics · 2025Review
- The LILRB family in hematologic malignancies: prognostic associations, mechanistic considerations, and therapeutic implications.Biomarker research · 2024Review
- Bone-marrow-homing lipid nanoparticles for genome editing in diseased and malignant haematopoietic stem cells.Nature nanotechnology · 2024Article
- Inhibiting AGTR1 reduces AML burden and protects the heart from cardiotoxicity in mouse models.Science translational medicine · 2024Article
- Kinome expression profiling improves risk stratification and therapeutic targeting in myelodysplastic syndromes.Blood advances · 2024Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Conventional strategies are not particularly successful in the treatment of leukaemia, and identification of signalling pathways crucial to the activity of leukaemia stem cells will provide targets for the development of new therapies. Here we report that certain receptors containing the immunoreceptor tyrosine-based inhibition motif (ITIM) are crucial for the development of acute myeloid leukaemia (AML). Inhibition of expression of the ITIM-containing receptor LAIR1 does not affect normal haematopoiesis but abolishes leukaemia development. LAIR1 induces activation of SHP-1, which acts as a phosphatase-independent signalling adaptor to recruit CAMK1 for activation of downstream CREB in AML cells. The LAIR1-SHP-1-CAMK1-CREB pathway sustains the survival and self-renewal of AML stem cells. Intervention in the signalling initiated by ITIM-containing receptors such as LAIR1 may result in successful treatment of AML.
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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.