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  • Macrophage migration inhibitory factor is required for NLRP3 inflammasome activation

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    Stanisic183801.pdf (1.142Mb)
    Author(s)
    Lang, Tali
    Lee, Jacinta PW
    Elgass, Kirstin
    Pinar, Anita A
    Tate, Michelle D
    Aitken, Elizabeth H
    Fan, Huapeng
    Creed, Sarah J
    Deen, Nadia S
    Traore, Daouda AK
    Mueller, Ivo
    Stanisic, Danielle
    Baiwog, Francesca S
    Skene, Colin
    Wilce, Matthew CJ
    Mansell, Ashley
    Morand, Eric F
    Harris, James
    Griffith University Author(s)
    Stanisic, Danielle
    Year published
    2018
    Metadata
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    Abstract
    Macrophage migration inhibitory factor (MIF) exerts multiple effects on immune cells, as well as having functions outside the immune system. MIF can promote inflammation through the induction of other cytokines, including TNF, IL-6, and IL-1 family cytokines. Here, we show that inhibition of MIF regulates the release of IL-1α, IL-1β, and IL-18, not by affecting transcription or translation of these cytokines, but via activation of the NLRP3 inflammasome. MIF is required for the interaction between NLRP3 and the intermediate filament protein vimentin, which is critical for NLRP3 activation. Further, we demonstrate that MIF ...
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    Macrophage migration inhibitory factor (MIF) exerts multiple effects on immune cells, as well as having functions outside the immune system. MIF can promote inflammation through the induction of other cytokines, including TNF, IL-6, and IL-1 family cytokines. Here, we show that inhibition of MIF regulates the release of IL-1α, IL-1β, and IL-18, not by affecting transcription or translation of these cytokines, but via activation of the NLRP3 inflammasome. MIF is required for the interaction between NLRP3 and the intermediate filament protein vimentin, which is critical for NLRP3 activation. Further, we demonstrate that MIF interacts with NLRP3, indicating a role for MIF in inflammasome activation independent of its role as a cytokine. These data advance our understanding of how MIF regulates inflammation and identify it as a factor critical for NLRP3 inflammasome activation.
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    Journal Title
    NATURE COMMUNICATIONS
    Volume
    9
    DOI
    https://doi.org/10.1038/s41467-018-04581-2
    Copyright Statement
    © 2018 The Authors. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
    Subject
    Multidisciplinary
    Publication URI
    http://hdl.handle.net/10072/383707
    Collection
    • Journal articles

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