ArticleEuropean journal of immunology2015
NLRC5 interacts with RIG-I to induce a robust antiviral response against influenza virus infection.
Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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Who cites it
37 citing papers in PubMed, 59 citations in OpenAlex.
- NLRC5 restricts Japanese encephalitis virus replication and neuroinflammation by interacting with the viral NS3 protein in an IFN-γ-dependent manner.Journal of neuroinflammation · 2026Article
- Role of PANoptosis in intestinal diseases and its therapeutic implications.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Sec8: a novel positive regulator of RIG-I in anti-RNA viral defense.Cell death & disease · 2026Article
- Article
- DUSP11 is an Intracellular Innate Immune Checkpoint in Lung Adenocarcinoma.Cancer immunology research · 2025Article
- New insights into the structure domain and function of NLR family CARD domain containing 5.Cell communication and signaling : CCS · 2025Review
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- A tale of endurance: bats, viruses and immune dynamics.Future microbiology · 2024Review
- Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look.Frontiers in immunology · 2024Review
- Several cell-intrinsic effectors drive type I interferon-mediated restriction of HIV-1 in primary CD4Cell reports · 2023Article
- NLRC5 restricts dengue virus infection by promoting the autophagic degradation of viral NS3 through E3 ligase CUL2 (cullin 2).Autophagy · 2023Article
- Teleost NOD-like receptors and their downstream signaling pathways: A brief review.Fish and shellfish immunology reports · 2022Review
- Review
- Coronavirus Porcine Deltacoronavirus Upregulates MHC Class I Expression through RIG-I/IRF1-Mediated NLRC5 Induction.Journal of virology · 2022Article
- Prolonged viral shedding prediction on non-hospitalized, uncomplicated SARS-CoV-2 patients using their transcriptome data.Computer methods and programs in biomedicine update · 2022Article
- NLRC5 regulates expression of MHC-I and provides a target for anti-tumor immunity in transmissible cancers.Journal of cancer research and clinical oncology · 2021Article
- Nod-Like Receptors in Host Defence and Disease at the Epidermal Barrier.International journal of molecular sciences · 2021Review
- Review
- The MHC Class-I Transactivator NLRC5: Implications to Cancer Immunology and Potential Applications to Cancer Immunotherapy.International journal of molecular sciences · 2021Review
- Role of NLRs in the Regulation of Type I Interferon Signaling, Host Defense and Tolerance to Inflammation.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 4 countries.
Funding
Abstract
The NLR protein, NLRC5 is an important regulator of MHC class I gene expression, however, the role of NLRC5 in other innate immune responses is less well defined. In the present study, we report that NLRC5 binds RIG-I and that this interaction is critical for robust antiviral responses against influenza virus. Overexpression of NLRC5 in the human lung epithelial cell line, A549, and normal human bronchial epithelial cells resulted in impaired replication of influenza virus A/Puerto Rico/8/34 virus (PR8) and enhanced IFN-β expression. Influenza virus leads to induction of IFN-β that drives RIG-I and NLRC5 expression in host cells. Our results suggest that NLRC5 extends and stabilizes influenza virus induced RIG-I expression and delays expression of the viral inhibitor protein NS1. We show that NS1 binds to NLRC5 to suppress its function. Interaction domain mapping revealed that NLRC5 interacts with RIG-I via its N-terminal death domain and that NLRC5 enhanced antiviral activity in an leucine-rich repeat domain independent manner. Taken together, our findings identify a novel role for NLRC5 in RIG-I-mediated antiviral host responses against influenza virus infection, distinguished from the role of NLRC5 in MHC class I gene regulation.
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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.