Macrophage migration inhibitory factor is required for NLRP3 inflammasome activation

Tali Lang, Jacinta P. W. Lee, Kirstin Elgass, Anita A. Pinar, Michelle D. Tate, Elizabeth H. Aitken, Huapeng Fan, Sarah J. Creed, Nadia S. Deen, Daouda A. K. Traore, Ivo Mueller, Danielle Stanisic, Francesca S. Baiwog, Colin Skene, Matthew C. J. Wilce, Ashley Mansell, Eric F. Morand and James Harris ()
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Tali Lang: Monash University
Jacinta P. W. Lee: Monash University
Kirstin Elgass: Hudson Institute of Medical Research
Anita A. Pinar: Monash University
Michelle D. Tate: Hudson Institute of Medical Research
Elizabeth H. Aitken: University of Melbourne
Huapeng Fan: Monash University
Sarah J. Creed: Hudson Institute of Medical Research
Nadia S. Deen: Monash University
Daouda A. K. Traore: Monash University
Ivo Mueller: Walter and Eliza Hall Institute, Parkville
Danielle Stanisic: Institute of Medical Research
Francesca S. Baiwog: Papua New Guinea Institute of Medical Research
Colin Skene: University of Melbourne
Matthew C. J. Wilce: Monash University
Ashley Mansell: Hudson Institute of Medical Research
Eric F. Morand: Monash University
James Harris: Monash University

Nature Communications, 2018, vol. 9, issue 1, 1-15

Abstract: 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 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.

Date: 2018
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DOI: 10.1038/s41467-018-04581-2

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