Post-translational modifications of NLRP3: to prime or not to prime? The NLRP3 inflammasome plays a central role in host defense against microbial infections but also contributes to inflammatory diseases. Functioning of…

#ThatIsTheQuestion Post-translational modifications of NLRP3: to prime or not to prime? Thrilled to have had the opportunity to write this review with @lozanzi.bsky.social 🤩! We discuss how PTMs coordinate during priming to control NLRP3 stability, location & partners. tinyurl.com/35dy5rcc

RNA N-glycosylation enables immune evasion and homeostatic efferocytosis by chemically caging acp3U. Excited to report this work lead by Vinnie @vinnieviruses.bsky.social and in collaboration with @vijayrathinam.bsky.social in @nature.com www.nature.com/articles/s41...

Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections Upon pathogen detection, phagocytes trigger immunity. This process induces tissue stress and the formation of host-derived molecules that further tune immune responses. We show that host-derived oxidi...

#EpigeneticPower! 💥 #NewPaperAlert! We show @cp-immunity.bsky.social that endogenous oxidized lipids decide whether host survives or dies during #sepsis, #ARDS, or Staph infection! Ox lipids bind & inhibit #AKT, boosting inhibitory H3K27 methylation via EZH2 & blocking #IL10!

Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections Upon pathogen detection, phagocytes trigger immunity. This process induces tissue stress and the formation of host-derived molecules that further tune immune responses. We show that host-derived oxidized phospholipids accumulate upon microbial encounter, epigenetically suppress IL-10, and exacerbate harmful inflammation. Thus, targeting oxPLs represents a therapeutic strategy to treat deranged inflammation after infection.

Online now: Epigenetic silencing of interleukin-10 by host-derived oxidized phospholipids supports a lethal inflammatory response to infections

Many thanks to you and your team @sunnyshinlab.bsky.social for your contribution. It was a pleasure working with you!

Many thanks for your insightful chapter Mikel!

We hope you find our new book informative and inspiring for your #immunometabolism studies!

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@lozanzi.bsky.social @bostonchildrens.bsky.social @harvardmed.bsky.social, Doug Green @stjude.bsky.social, @alexhooftman.bsky.social @EPFL, Clovis Palmer @tulaneu.bsky.social, Ana Domingos @ox.ac.uk, and contributions from myself, Zbigniew Zasłona and
@lukeanthonyoneill.bsky.social.

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Our book includes chapters from the labs of Alice Prince @columbiauniversity.bsky.social, @sunnyshinlab.bsky.social & @metabailism.bsky.social @upenn.edu, Fiachra Humphries @umasschan.bsky.social, Jonathan Powell @CalicoLifeSciences, @emday4.bsky.social @westernu.ca,

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With many thanks to all authors for their generous and detailed contributions, and all the team @elsevierconnect.bsky.social for their support in publishing the book.

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In this new book, we and leaders in the field summarize the recent history of the ever-growing field of immunometabolism, the current state of the field, and future directions including the generation of new therapies harnessing and targeting immunometabolism.

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Are you interested in #immunometabolism but not sure where to start?

Introducing our new book “Metabolites as Signals in Immunity and Inflammation”, co-edited with Zbigniew Zasłona and @lukeanthonyoneill.bsky.social (@tcddublin.bsky.social), available now.

shop.elsevier.com/books/metabo...

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Immunothrombolytic monocyte-neutrophil axes dominate the single-cell landscape of human thrombosis and correlate with thrombus resolution Thrombotic diseases remain the major cause of death and disability worldwide, and the contribution of inflammation is increasingly recognized. Thrombo…

Immune cells contribute to thrombosis in mouse models - but what about human disease? We used scRNA Sequencing, flow cytometry and histology to better understand immune cells in human stroke thrombi www.sciencedirect.com/science/arti... now online @cp-immunity.bsky.social

Aging platelets shift their hemostatic properties to inflammatory functions Key PointsPlatelets change their phenotype as they age in circulation, skewing toward inflammatory function over time.Genetic models of increased platelet

Very happy to contribute another @bloodjournal.bsky.social cover with our story on aging platelets:
ashpublications.org/blood/articl...
Thoughtful commentary by Laura Gutiérrez in the issue as well.

Epidermal ZBP1 stabilizes mitochondrial Z-DNA to drive UV-induced IFN signaling in autoimmune photosensitivity ZBP1 and mitochondrial Z-DNA drive autoimmune photosensitivity via cGAS-STING activation.

#InterferonFriendOrFoe?! Klein @kahlenberglab.bsky.social &co show Science Immunology that UV drives mitochondrial Z-DNA to induce type I & III IFNs in keratinocytes. IFN-I upregulates ZBP1 that binds Z-DNA activating cGAS-STING to boost IFNs, photosensitivity & inflammation in #Lupus skin!

Pleased to share our latest paper in Science Advances on myeloid cell ‘trained hypercoagulability’! 🚀 Project led by @aislingrehill.bsky.social - huge thanks to our collaborators & funders @tcddublin.bsky.social @researchireland.bsky.social CHI and HRB Ireland tinyurl.com/df4fsrrx

Macrophages recycle phagocytosed bacteria to fuel immunometabolic responses - Nature Phagocytosed bacteria can serve as an alternative nutrient source for macrophages, influencing their metabolic and immune responses through the recycling of microbial components, with the process regu...

#WeekendRead! #WeAreWhatWeEat! Lesbats, Garaude &co show @nature.com that macrophages recycle phagocytosed bacteria to fuel their metabolism but that dead, compared to live, bacteria still feed macrophages but reduce the induction of ROS & the secretion of IL1b! www.nature.com/articles/s41...

Leaving Boston in a few days after a productive time in the Zanoni Lab at @bostonchildrens.bsky.social and Harvard Medical School. Huge thanks to Ivan @lozanzi.bsky.social and the whole lab for their support and inspiration. I will miss you all! Excited to keep working together on cool science! 🤩