ArticleCellular oncology (Dordrecht, Netherlands)2024
LILRB2 promotes immune escape in breast cancer cells via enhanced HLA-A degradation.
Article in Cellular oncology (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Identification of basement membrane-based prognostic signature and potential therapeutic drugs in hepatocellular carcinoma.Translational cancer research · 2025Article
- SPI1 upregulated LILRB2 to enhance the immunosuppressive phenotype of LPS-tolerant macrophages by inhibiting TLR8-mediated MyD88/NF-κB signaling.Biology direct · 2025Article
- Changing landscape of hematopoietic and mesenchymal cells and their interactions during aging and in age-related skeletal pathologies.Mechanisms of ageing and development · 2025Review
- Development of a prognostic model based on four genes related to exhausted CD8+ T cell in triple-negative breast cancer patients: a comprehensive analysis integrating scRNA-seq and bulk RNA-seq.Discover oncology · 2025Article
- Targeting ILT4 to Improve Immunotherapy Efficacy in Solid Tumour: From Bench to Bedside.ImmunoTargets and therapy · 2025Review
- Inhibitory leukocyte immunoglobulin-like receptors, subfamily B (LILRBs) in human diseases: structure, roles, mechanisms, and clinical applications.Theranostics · 2025Review
- Exploring Core Genes Associated with Sepsis and Systemic Inflammatory Response Syndrome Using Single-Cell Sequencing Technology.Journal of inflammation research · 2025Article
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Authors and funding
17 authors at 5 institutions in 2 countries.
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Abstract
purposeIncreased expression of leukocyte immunoglobulin-like receptor subfamily B member 2 (LILRB2) is associated with immune evasion in breast cancer (BC). The aim of this study to elucidate the role of LILRB2 in BC progression.
methodsLILRB2 expression in tumor tissues was detected by immunohistochemical staining. Human leukocyte antigen A (HLA-A) expression in BC cells was detected by Western blotting, and HLA-A ubiquitination was detected by immunoprecipitation and histidine pulldown assay. An in-situ tumor model was established in nude BALB/c mice to verify the role of LILRB2 in immune escape. Finally, the functions and potential mechanisms of LILRB2 in BC progression were explored using in silico data.
resultsLILRB2 was upregulated in BC tissues and cells, and correlated positively with poor prognosis. LILRB2 promoted BC progression by downregulating HLA-A expression. Mechanistically, LILRB2 facilitates the ubiquitination and subsequent degradation of HLA-A by promoting the interaction between the ubiquitin ligase membrane-associated ring finger protein 9 (MARCH9) and HLA-A. In syngeneic graft mouse models, LILRB2-expressing BC cells evaded CD8 + T cells and inhibited the secretion of cytokines by the cytotoxic CD8 + T cells.
conclusionLILRB2 downregulates HLA-A to promote immune evasion in BC cells and is a promising new target for BC treatment.
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