ArticleImmunity2009
Structure of natural killer cell receptor KLRG1 bound to E-cadherin reveals basis for MHC-independent missing self recognition.
Article in Immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 106 citations in OpenAlex.
- CD39Science translational medicine · 2026Article
- E-cadherin expression promotes tumor growth via KLRG1-dependent pathways.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- IDH1 Mutant Glioma Favors Group 3 Innate Lymphoid Cells and Is Resistant to Immune Checkpoint Expression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Association between T cell exhaustion and the recurrence of atrial fibrillation after cryoballoon ablation.Frontiers in immunology · 2026Article
- Investigation of the toxicological effects of PFAS on cholangiocarcinoma based on network toxicology, bioinformatics, and molecular docking.Scientific reports · 2025Article
- Tumor microbiome: roles in tumor initiation, progression, and therapy.Molecular biomedicine · 2025Review
- Recognition of Self and Viral Ligands by NK Cell Receptors.Immunological reviews · 2025Review
- Review
- The role of KLRG1: a novel biomarker and new therapeutic target.Cell communication and signaling : CCS · 2024Review
- Secondary Sites of the C-type Lectin-Like Fold.Chemistry (Weinheim an der Bergstrasse, Germany) · 2024Review
- KLRG1-expressing CD8+ T cells are exhausted and polyfunctional in patients with chronic hepatitis B.PloS one · 2024Article
- KLRG1 expression on natural killer cells is associated with HIV persistence, and its targeting promotes the reduction of the viral reservoir.Cell reports. Medicine · 2023Article
- Emerging Nano-/Biotechnology Drives Oncolytic Virus-Activated and Combined Cancer Immunotherapy.Research (Washington, D.C.) · 2023Article
- Sex differences exist in adult heart group 2 innate lymphoid cells.BMC immunology · 2022Article
- N-cadherin protects oral cancer cells from NK cell killing in the circulation by inducing NK cell functional exhaustion via the KLRG1 receptor.Journal for immunotherapy of cancer · 2022Article
- Structure of the human NK cell NKR-P1:LLT1 receptor:ligand complex reveals clustering in the immune synapse.Nature communications · 2022Article
- Article
- The Immunogenetics of Autoimmune Blistering Diseases.Advances in experimental medicine and biology · 2022Review
- The Yin and Yang of Targeting KLRG1Frontiers in immunology · 2022Review
- Glioblastoma microenvironment and its reprogramming by oncolytic virotherapy.Frontiers in cellular neuroscience · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
The cytolytic activity of natural killer (NK) cells is regulated by inhibitory receptors that detect the absence of self molecules on target cells. Structural studies of missing self recognition have focused on NK receptors that bind MHC. However, NK cells also possess inhibitory receptors specific for non-MHC ligands, notably cadherins, which are downregulated in metastatic tumors. We determined the structure of killer cell lectin-like receptor G1 (KLRG1) in complex with E-cadherin. KLRG1 mediates missing self recognition by binding to a highly conserved site on classical cadherins, enabling it to monitor expression of several cadherins (E-, N-, and R-) on target cells. This site overlaps the site responsible for cell-cell adhesion but is distinct from the integrin alpha(E)beta(7) binding site. We propose that E-cadherin may coengage KLRG1 and alpha(E)beta(7) and that KLRG1 overcomes its exceptionally weak affinity for cadherins through multipoint attachment to target cells, resulting in inhibitory signaling.
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What OpenQuestion holds
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.