ArticleThe Journal of experimental medicine2010
Identification of a polyI:C-inducible membrane protein that participates in dendritic cell-mediated natural killer cell activation.
Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 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.
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Who cites it
48 citing papers in PubMed, 98 citations in OpenAlex.
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- Toll-like receptors (TLRs): An old family of immune receptors with a new face in cancer pathogenesis.Journal of cellular and molecular medicine · 2021Review
- Unveiling the Physical and Functional Niches of FAM26F by Analyzing Its Subcellular Localization and Novel Interacting Partners.ACS omega · 2020Article
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- TLR3 Expression Induces Apoptosis in Human Non-Small-Cell Lung Cancer.International journal of molecular sciences · 2020Article
- Interferon regulatory factor 3 plays a role in macrophage responses to interferon-γ.Immunobiology · 2019Article
- Inflammation and Liver Cancer: Molecular Mechanisms and Therapeutic Targets.Seminars in liver disease · 2019Review
- Toll-Like Receptors as Therapeutic Targets in Central Nervous System Tumors.BioMed research international · 2019Review
- Toll-like receptors in immunity and inflammatory diseases: Past, present, and future.International immunopharmacology · 2018Review
- Turn Back the TIMe: Targeting Tumor Infiltrating Myeloid Cells to Revert Cancer Progression.Frontiers in immunology · 2018Review
- Type I Interferons and Natural Killer Cell Regulation in Cancer.Frontiers in immunology · 2017Review
- Significant role for IRF3 in both T cell and APC effector functions during T cell responses.Cellular immunology · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In myeloid dendritic cells (mDCs), TLR3 is expressed in the endosomal membrane and interacts with the adaptor toll/interleukin 1 receptor homology domain-containing adaptor molecule 1 (TICAM-1; TRIF). TICAM-1 signals culminate in interferon (IFN) regulatory factor (IRF) 3 activation. Co-culture of mDC pretreated with the TLR3 ligand polyI:C and natural killer (NK) cells resulted in NK cell activation. This activation was triggered by cell-to-cell contact but not cytokines. Using expression profiling and gain/loss-of-function analyses of mDC genes, we tried to identify a TICAM-1-inducing membrane protein that participates in mDC-mediated NK activation. Of the nine candidates screened, one contained a tetraspanin-like sequence and satisfied the screening criteria. The protein, referred to as IRF-3-dependent NK-activating molecule (INAM), functioned in both the mDC and NK cell to facilitate NK activation. In the mDC, TICAM-1, IFN promoter stimulator 1, and IRF-3, but not IRF-7, were required for mDC-mediated NK activation. INAM was minimally expressed on NK cells, was up-regulated in response to polyI:C, and contributed to mDC-NK reciprocal activation via its cytoplasmic tail, which was crucial for the activation signal in NK cells. Adoptive transfer of INAM-expressing mDCs into mice implanted with NK-sensitive tumors caused NK-mediated tumor regression. We identify a new pathway for mDC-NK contact-mediated NK activation that is governed by a TLR signal-derived membrane molecule.
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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.