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The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Influenza virus activates inflammasomes via its intracellular M2 ion channel

Open access
Ichinohe, Takeshi, Pang, Iris K, Iwasaki, Akiko·2010·Nature Immunology

Abstract

Influenza virus, a negative-stranded RNA virus that causes severe illness in humans and animals, stimulates the inflammasome through the Nod-like receptor NLRP3. However, the mechanism by which influenza virus activates the NLRP3 inflammasome is unknown. Here we show that the influenza virus M2 protein, a proton-selective ion channel important in viral pathogenesis, stimulates the NLRP3 inflammasome pathway. M2 channel activity was required for the activation of inflammasomes by influenza and was sufficient to activate inflammasomes in primed macrophages and dendritic cells. M2-induced activation of inflammasomes required its localization to the Golgi apparatus and was dependent on the pH gradient. Our results show a mechanism by which influenza virus infection activates inflammasomes and identify the sensing of disturbances in intracellular ionic concentrations as a previously unknown pathogen-recognition pathway.

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Metadata

Authors
Ichinohe, T., Pang, I. K., & Iwasaki, A.
Venue
Nature Immunology
Published
2010-04-11
Volume
11
Issue
5
Pages
404-410
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
OpenAlex
W2158939742
Cited by
631
References
11
FWCI
19.14
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Influenza virus activates inflammasomes via its intracellular M2 ion channel. https://app.cochat.ai/papers/10.1038/ni.1861
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Ichinohe, T., Pang, I. K., & Iwasaki, A. (2010). Influenza virus activates inflammasomes via its intracellular M2 ion channel. Nature Immunology. https://doi.org/10.1038/ni.1861

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.