ArticleFrontiers in immunology2018
Ig-Like Transcript 2 (ILT2) Blockade and Lenalidomide Restore NK Cell Function in Chronic Lymphocytic Leukemia.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 44 citations in OpenAlex.
- Neoadjuvant atezolizumab for resectable non-small cell lung cancer: an open-label, single-arm phase II trial.Nature medicine · 2022Trial
- Structural mechanism of anti-MHC-I antibody blocking of inhibitory NK cell receptors in tumor immunity.Communications biology · 2026Article
- Antibody-Mediated Inhibition of HLA/LILR Interactions Breaks Innate Immune Tolerance and Induces Antitumor Immunity.Cancer immunology research · 2025Article
- Structural mechanism of anti-MHC-I antibody blocking of inhibitory NK cell receptors in tumor immunity.Research square · 2025Article
- miR-155-5p Silencing Does Not Alter BTLA Molecule Expression in CLL T Cells: Implications for Targeted Immunotherapy.Biomolecules · 2025Article
- LILRB1 enhances the progression of diffuse large B-cell lymphoma through the CREB-SORBS3 pathway.Cellular oncology (Dordrecht, Netherlands) · 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
- The role of exhausted natural killer cells in the immunopathogenesis and treatment of leukemia.Cell communication and signaling : CCS · 2024Review
- Inhibitory receptors of plasmacytoid dendritic cells as possible targets for checkpoint blockade in cancer.Frontiers in immunology · 2024Review
- MHC1/LILRB1 axis as an innate immune checkpoint for cancer therapy.Frontiers in immunology · 2024Review
- Immune Evasion Through Human Leukocyte Antigen Implications and Its Impact on Targeted Therapy.Cureus · 2024Review
- BTLA dysregulation correlates with poor outcome and diminished T cell-mediated antitumor responses in chronic lymphocytic leukemia.Cancer immunology, immunotherapy : CII · 2023Article
- Immunoglobulin-like transcript 2 blockade restores antitumor immune responses in glioblastoma.Cancer science · 2023Article
- Human leukocyte immunoglobulin-like receptors in health and disease.Frontiers in immunology · 2023Review
- Perspectives of targeting LILRB1 in innate and adaptive immune checkpoint therapy of cancer.Frontiers in immunology · 2023Review
- Natural Killer Cells in Chronic Lymphocytic Leukemia: Functional Impairment and Therapeutic Potential.Cancers · 2022Review
- Blockade of novel immune checkpoints and new therapeutic combinations to boost antitumor immunity.Journal of experimental & clinical cancer research : CR · 2022Review
- Dual checkpoint blockade of CD47 and LILRB1 enhances CD20 antibody-dependent phagocytosis of lymphoma cells by macrophages.Frontiers in immunology · 2022Article
- Mechanisms for Host Immune Evasion Mediated byFrontiers in immunology · 2022Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the cardinal features of chronic lymphocytic leukemia (CLL) is its association with a profound immunosuppression. NK cell function is markedly impaired in CLL patients, who show a significant dysregulation of the expression of activating and inhibitory receptors. Here, we analyzed the role of the novel inhibitory receptor Ig-like transcript 2 (ILT2, also termed LIR-1, LILRB1) in the regulation of NK cells in CLL. Our results show that ILT2 expression was significantly decreased on leukemic cells and increased on NK cells of CLL patients, particularly in those with advanced disease and with bad prognostic features, such as those carrying chromosome del(11q). The immunomodulatory drug lenalidomide may regulate the expression of ILT2 and its ligands in CLL since it significantly increased the expression of ILT2 and partially reestablished the expression of its ligands on leukemic cells. Furthermore, lenalidomide significantly increased the activation and proliferation of NK cells, which was strongly enhanced by ILT2 blockade. Combining ILT2 blockade and lenalidomide activated NK cell cytotoxicity resulting in increased elimination of leukemic cells from CLL patients. Overall, we describe herein the role of an inhibitory receptor involved in the suppression of NK cell activity in CLL, which is restored by ILT2 blockade in combination with lenalidomide, suggesting that it may be an interesting therapeutic strategy to be explored in this disease.
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