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Immunity
Article
License: Elsevier Non-Commercial
Data sources: UnpayWall
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Immunity
Article . 2009
License: Elsevier Non-Commercial
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Immunity
Article . 2009 . Peer-reviewed
License: Elsevier Non-Commercial
Data sources: Crossref
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Virus Binding to a Plasma Membrane Receptor Triggers Interleukin-1α-Mediated Proinflammatory Macrophage Response In Vivo

Authors: Di Paolo, Nelson C.; Miao, Edward A.; Iwakura, Yoichiro; Murali-Krishna, Kaja; Aderem, Alan; Flavell, Richard A.; Papayannopoulou, Thalia; +1 Authors

Virus Binding to a Plasma Membrane Receptor Triggers Interleukin-1α-Mediated Proinflammatory Macrophage Response In Vivo

Abstract

The recognition of viral components by host pattern-recognition receptors triggers the induction of the antiviral innate immune response. Toll-like receptor 9 (TLR9) and NLRP3 inflammasome were shown to be the principal specific sensors of viral double-stranded DNA. Here we present evidence that macrophages in vivo activated an innate immune response to a double-stranded DNA virus, adenovirus (Ad), independently of TLR9 or NLRP3 inflammasome. In response to Ad, macrophage-derived IL-1 alpha triggered IL-1RI-dependent production of a defined set of proinflammatory cytokines and chemokines. The IL-1 alpha-mediated response required a selective interaction of virus arginine-glycine-aspartic acid (RGD) motifs with macrophage beta(3) integrins. Thus, these data identify IL-1 alpha-IL-1RI as a key pathway allowing for the activation of proinflammatory responses to the virus, independently of its genomic nucleic acid recognition.

Keywords

Mice, Knockout, MICROBIO, Macrophages, Immunology, Genetic Vectors, Integrin beta3, Receptors, Interleukin-1, Immunity, Innate, Adenoviridae, Mice, Inbred C57BL, Mice, Infectious Diseases, CELLIMMUNO, Interleukin-1alpha, Toll-Like Receptor 9, NLR Family, Pyrin Domain-Containing 3 Protein, Immunology and Allergy, Animals, MOLIMMUNO, Carrier Proteins, Spleen

  • BIP!
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    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    178
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 1%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 1%
Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
178
Top 1%
Top 10%
Top 1%
hybrid