ReviewImmunological reviews2006
Activation, coactivation, and costimulation of resting human natural killer cells.
Review in Immunological reviews, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05933070 (A Phase I Open-Label Dose Escalation Study Of Intravenous INKmune In Patients With Myelodysplastic Syndrome With Excess Blasts), which is not on this map. Cited by 320 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
A Phase I Open-Label Dose Escalation Study Of Intravenous INKmune In Patients With Myelodysplastic Syndrome With Excess Blasts (MDS-EB-1/2 - MDS-CMML 1/2) Or Acute Myeloid Leukaemia (AML)
Who cites it
320 citing papers in PubMed, 3 syntheses or guidelines pooled it, 636 citations in OpenAlex.
- Natural Killer Cell-Derived Extracellular Vesicles as a Promising Immunotherapeutic Strategy for Cancer: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- The soldiers needed to be awakened: Tumor-infiltrating immune cells.Frontiers in genetics · 2022Pooled it
- Phenotypical and potential functional characteristics of different immune cells expressing CD28H/B7-H5 and their relationship with cancer prognosis.Clinical and experimental immunology · 2020Pooled it
- Autoantibodies to Killer Cell Immunoglobulin-Like Receptors in Patients With Systemic Lupus Erythematosus Induce Natural Killer Cell Hyporesponsiveness.Frontiers in immunology · 2019Trial
- Article
- EGFRxCD16 bispecific antibodies orchestrate superior NK cell-mediated lysis of ovarian cancer and NSCLC cell lines in combination with oncolytic viruses.Cancer immunology, immunotherapy : CII · 2026Article
- BAP1 loss impairs IFN-γ signaling and enhances NK cell-mediated cytotoxicity in myeloid leukemia.Cancer immunology, immunotherapy : CII · 2026Article
- YTHDF2 in inflammation: Mechanisms and therapeutic strategies.Genes & diseases · 2026Review
- The role of long non-coding RNAs in NK cell biology and diseases.Genes & diseases · 2026Review
- Large-scale generation of iNK and CAR-iNK cells from CD34Nature biomedical engineering · 2026Article
- Retinoids enhance NK effector function against HIV-infected CD4 T cells.Journal of virology · 2026Article
- Programmable iPSC-derived CAR-NK vesicles remodel the immune microenvironment and eradicate tumors.Cell reports. Medicine · 2026Article
- Innate immune cells in chimeric antigen receptor therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Review
- IL-7Rα signaling potentiates the anti-tumor activity of NK92 cells.Frontiers in immunology · 2026Article
- Divergent on-target off-tumor effects by CAR T and CAR NK cells suggest different efficacy and safety of cell therapies.Oncoimmunology · 2025Article
- Integrating Single-Cell and Spatial Transcriptomics Reveals NK Cell Subpopulations Associated With Immunotherapy for Melanoma.Smart medicine · 2025Article
- Review
- NK and T cell evasion mechanism of human cytomegalovirus.Archives of virology · 2025Review
- Establishment of Immune-Evasive iPSCs from PBMCs Using B2M Knockout and CD47/HLA-E Overexpression.Tissue engineering and regenerative medicine · 2025Article
- CAR-engineered lymphocyte persistence is governed by a FAS ligand-FAS autoregulatory circuit.Nature cancer · 2025Article
260 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Natural killer (NK) cells possess potent perforin- and interferon-gamma-dependent effector functions that are tightly regulated. Inhibitory receptors for major histocompatibility complex class I display variegated expression among NK cells, which confers specificity to individual NK cells. Specificity is also provided by engagement of an array of NK cell activation receptors. Target cells may express ligands for a multitude of activation receptors, many of which signal through different pathways. How inhibitory receptors intersect different signaling cascades is not fully understood. This review focuses on advances in understanding how activation receptors cooperate to induce cytotoxicity in resting NK cells. The role of activating receptors in determining specificity and providing redundancy of target cell recognition is discussed. Using Drosophila insect cells as targets, we have examined the contribution of individual receptors. Interestingly, the strength of activation is not determined simply by additive effects of parallel activation pathways. Combinations of signals from different receptors can have different outcomes: synergy, no enhancement over individual signals, or additive effects. Cytotoxicity requires combined signals for granule polarization and degranulation. The integrin leukocyte function-associated antigen-1 contributes a signal for polarization but not for degranulation. Conversely, CD16 alone or in synergistic combinations, such as NKG2D and 2B4, signals for phospholipase-C-gamma- and phosphatidylinositol-3-kinase-dependent degranulation.
Indexed as
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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.