ArticleEMBO molecular medicine2024
LILRB1-HLA-G axis defines a checkpoint driving natural killer cell exhaustion in tuberculosis.
Article in EMBO molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Host-pathogen interactions in tuberculosis: from immunological mechanisms to translational applications.Cell insight · 2026Review
- Metagenomic Next-Generation Sequencing for Pulmonary Tuberculosis Diagnosis and Infection Risk Factor Analysis in AECOPD Patients: A Single-Center Retrospective Study.Journal of clinical medicine · 2026Article
- Targeting macrophage-driven NK cell immunosuppression to improve cancer immunotherapy.Journal for immunotherapy of cancer · 2026Review
- Trained immunity in respiratory diseases: Mechanisms of action and intervention strategies.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Immunotherapy for tuberculosis: emerging modalities, cross-disciplinary innovations, and roadmaps for drug-resistant disease.Frontiers in immunology · 2026Review
- LILRB1 Modulates Neutrophil Migration, NETosis, and Inflammation in Drug-ResistantInfection and drug resistance · 2026Article
- Research progress on the role and dysregulation of NK cells in anti-tuberculosis immunity.Frontiers in immunology · 2026Review
- Distribution of granzyme-expressing NK cells in tuberculosis reflects subset and compartment-specific remodeling.Frontiers in immunology · 2026Article
- Single-cell RNA sequencing reveals immune cell dysfunction and rewired interaction networks in the peripheral blood of active tuberculosis patients.BMC immunology · 2025Article
- Site-specific genome engineering of primary human natural killer cells for programmable anti-tumor function.bioRxiv : the preprint server for biology · 2025Article
- NK Cell Senescence in Cancer: From Molecular Mechanisms to Therapeutic Opportunities.Aging and disease · 2025Review
- NCAM1-SHIP2 axis upon recognizing microbes inhibits the expressions of inflammatory factors through P38-H3K4me and P38-NF-κB pathways in oyster.Cell communication and signaling : CCS · 2025Article
- Inhibitory leukocyte immunoglobulin-like receptors, subfamily B (LILRBs) in human diseases: structure, roles, mechanisms, and clinical applications.Theranostics · 2025Review
- Immune dysregulation in endometrial tuberculosis: elevated HLA-G and IL-1Ra as key modulators.Frontiers in cellular and infection microbiology · 2025Article
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Authors and funding
17 authors.
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Abstract
Chronic infections, including Mycobacterium tuberculosis (Mtb)-caused tuberculosis (TB), can induce host immune exhaustion. However, the key checkpoint molecules involved in this process and the underlying regulatory mechanisms remain largely undefined, which impede the application of checkpoint-based immunotherapy in infectious diseases. Here, through adopting time-of-flight mass cytometry and transcriptional profiling to systematically analyze natural killer (NK) cell surface receptors, we identify leukocyte immunoglobulin like receptor B1 (LILRB1) as a critical checkpoint receptor that defines a TB-associated cell subset (LILRB1
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