ArticleThe Journal of clinical investigation2018
LILRB1 polymorphisms influence posttransplant HCMV susceptibility and ligand interactions.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Natural killer cells against viral infection: from basic biology to immunotherapy.Precision clinical medicine · 2026Review
- Dual Blockade of LILRB1 and LILRB2 Enhances Antiviral Immune Responses in SIV Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Human Cytomegalovirus Immune Evasion of Natural Killer Cells: A Virus for All Seasons?Pathogens (Basel, Switzerland) · 2025Review
- Inhibitory leukocyte immunoglobulin-like receptors, subfamily B (LILRBs) in human diseases: structure, roles, mechanisms, and clinical applications.Theranostics · 2025Review
- Genetic variants of the HLA-G/LILRB1 ligand-receptor axis in donors or recipients are prognostic covariates for rejection after living kidney transplantation.Frontiers in immunology · 2025Article
- Article
- The impact of HLA polymorphism on herpesvirus infection and disease.Immunogenetics · 2023Review
- Local immune recognition of trophoblast in early human pregnancy: controversies and questions.Nature reviews. Immunology · 2023Review
- Elevated sHLA-G plasma levels post chemotherapy combined with ILT-2 rs10416697C allele status of the sHLA-G-related receptor predict poorest disease outcome in early triple-negative breast cancer patients.Frontiers in immunology · 2023Article
- Natural LILRB1 D1-D2 variants show frequency differences in populations and bind to HLA class I with various avidities.Immunogenetics · 2022Article
- HLA-E restricted cytomegalovirus UL40 peptide polymorphism may represent a risk factor following congenital infection.BMC genomics · 2022Article
- New Targets for Antiviral Therapy: Inhibitory Receptors and Immune Checkpoints on Myeloid Cells.Viruses · 2022Review
- Article
- LIR-1 educates expanded human NK cells and defines a unique antitumor NK cell subset with potent antibody-dependent cellular cytotoxicity.Clinical & translational immunology · 2021Article
- Leukocyte Immunoglobulin-Like Receptors in Regulating the Immune Response in Infectious Diseases: A Window of Opportunity to Pathogen Persistence and a Sound Target in Therapeutics.Frontiers in immunology · 2021Review
- Bioinformatics analyses on the immune status of renal transplant patients, a systemic research of renal transplantation.BMC medical genomics · 2020Article
- Assessing Anti-HCMV Cell Mediated Immune Responses in Transplant Recipients and Healthy Controls Using a Novel Functional Assay.Frontiers in cellular and infection microbiology · 2020Article
- NK Cells from RAG- or DCLRE1C-Deficient Patients Inhibit HCMV.Microorganisms · 2019Article
- The Evolutionary Arms Race between Virus and NK Cells: Diversity Enables Population-Level Virus Control.Viruses · 2019Review
- HCMV-Encoded NK Modulators: Lessons FromFrontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
20 authors at 9 institutions in 3 countries.
Funding
Abstract
UL18 is a human CMV (HCMV) MHC class I (MHCI) homolog that efficiently inhibits leukocyte immunoglobulin-like receptor subfamily B member 1 (LILRB1)+ NK cells. We found an association of LILRB1 polymorphisms in the regulatory regions and ligand-binding domains with control of HCMV in transplant patients. Naturally occurring LILRB1 variants expressed in model NK cells showed functional differences with UL18 and classical MHCI, but not with HLA-G. The altered functional recognition was recapitulated in binding assays with the binding domains of LILRB1. Each of 4 nonsynonymous substitutions in the first 2 LILRB1 immunoglobulin domains contributed to binding with UL18, classical MHCI, and HLA-G. One of the polymorphisms controlled addition of an N-linked glycan, and that mutation of the glycosylation site altered binding to all ligands tested, including enhancing binding to UL18. Together, these findings indicate that specific LILRB1 alleles that allow for superior immune evasion by HCMV are restricted by mutations that limit LILRB1 expression selectively on NK cells. The polymorphisms also maintained an appropriate interaction with HLA-G, fitting with a principal role of LILRB1 in fetal tolerance.
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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.