Macrophage migration inhibitory factor is required for NLRP3 inflammasome activation

Lang, T; Lee, JPW; Elgass, K; Pinar, AA; Tate, MD; Aitken, EH; FAN, H; Creed, SJ; Deen, NS; Traore, DAK; Mueller, I; Stanisic, D; Baiwog, FS; Skene, C; Wilce, MCJ; Mansell, A; MORAND, EF; Harris, J

Author(s): Lang, T; Lee, JPW; Elgass, K; Pinar, AA; Tate, MD; Aitken, EH; FAN, H; Creed, SJ; Deen, NS; Traore, DAK; Mueller, I; Stanisic, D; Baiwog, FS; Skene, C; Wilce, MCJ; Mansell, A; MORAND, EF; Harris, J;
Details: Publication Year 2018-06-08,Volume 9,Issue #1,Page 2223
Journal Title: Nature Communications
Publication Type: Journal Article
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-1alpha, IL-1beta, 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.
Publisher: Springer Nature
Research Division(s): Population Health And Immunity
PubMed ID: 29884801
Publisher's Version: https://doi.org/10.1038/s41467-018-04581-2
Open Access at Publisher's Site: https://doi.org/10.1038/s41467-018-04581-2
NHMRC Grants: NHMRC/1068040,
Terms of Use/Rights Notice: Refer to copyright notice on published article.
Documents: s41467-018-04581-2.pdf - (2.22MB, application/pdf)

Creation Date: 2018-06-26 12:34:44

Last Modified: 2018-06-26 01:40:22