Last chance to submit an abstract for this EMBO Workshop! Abstract submission deadline on February 15, registration deadline on March 1.

meetings.embo.org/event/26-pat...

#EMBO #immunity #host-pathogen #interferons #antiviral immunity

#Autoantibodies neutralizing type 1 #interferons in two cohorts of people with #HIV. New study from Julie A. Jensen, Jean-Laurent Casanova @casanovalab.bsky.social, Trine H. Mogensen @au.dk and colleagues: rupress.org/jhi/article/...

@esidsociety.bsky.social

Top: Type III interferon alters the nuclear localization of the transcriptional co-regulator YAP during wound healing of human bronchial epithelial cells. Micrographs show localization or YAP (red) relative to the cell nucleus (blue) in cells adjacent to a scratch in the monolayer (dark area, right of images). In untreated cultures, YAP is present in most nuclei (purple nuclei, left panel) whereas in the presence of Type III interferon, the percentage of cells with nuclear YAP is greatly reduced (blue nuclei, right panel). Image credit: Krupakar Subramaniam. Bottom: Model. Type III and Type I IFN receptor signaling activate LATS1 to curtail tissue repair during acute viral infection. Left-hand panel: During acute viral infection, high concentrations of Type III and/or Type I IFN receptor signaling trigger JAK-dependent, STAT1-independent phosphorylation of LATS1, leading to phosphorylation and degradation of YAP and reduced tissue repair activities mediated by YAP target genes. In rapidly proliferating cell types, active LATS1/2 also blocks repair in part via a p53-dependent mechanism. Right-hand panel: During resolution of viral infection, lower concentrations of Type III and/or Type I IFN may continue to activate STAT1-mediated antiviral defenses but no longer activate LATS1/2, allowing epithelial repair to resume.

#Interferons protect against #ViralInfection, but can hinder tissue repair - how? @ellenfoxman.bsky.social &co show that high IFN levels suppress #BronchialCell migration & proliferation during tissue repair via JAK-driven LATS1 activation, independent of STAT1 @plosbiology.org 🧪 plos.io/4k1pyKA

Top: Type III interferon alters the nuclear localization of the transcriptional co-regulator YAP during wound healing of human bronchial epithelial cells. Micrographs show localization or YAP (red) relative to the cell nucleus (blue) in cells adjacent to a scratch in the monolayer (dark area, right of images). In untreated cultures, YAP is present in most nuclei (purple nuclei, left panel) whereas in the presence of Type III interferon, the percentage of cells with nuclear YAP is greatly reduced (blue nuclei, right panel). Image credit: Krupakar Subramaniam. Bottom: Model. Type III and Type I IFN receptor signaling activate LATS1 to curtail tissue repair during acute viral infection. Left-hand panel: During acute viral infection, high concentrations of Type III and/or Type I IFN receptor signaling trigger JAK-dependent, STAT1-independent phosphorylation of LATS1, leading to phosphorylation and degradation of YAP and reduced tissue repair activities mediated by YAP target genes. In rapidly proliferating cell types, active LATS1/2 also blocks repair in part via a p53-dependent mechanism. Right-hand panel: During resolution of viral infection, lower concentrations of Type III and/or Type I IFN may continue to activate STAT1-mediated antiviral defenses but no longer activate LATS1/2, allowing epithelial repair to resume.

#Interferons protect against #ViralInfection, but can hinder tissue repair - how? @ellenfoxman.bsky.social &co show that high IFN levels suppress #BronchialCell migration & proliferation during tissue repair via JAK-driven LATS1 activation, independent of STAT1 @plosbiology.org 🧪 plos.io/4k1pyKA

Top: Type III interferon alters the nuclear localization of the transcriptional co-regulator YAP during wound healing of human bronchial epithelial cells. Micrographs show localization or YAP (red) relative to the cell nucleus (blue) in cells adjacent to a scratch in the monolayer (dark area, right of images). In untreated cultures, YAP is present in most nuclei (purple nuclei, left panel) whereas in the presence of Type III interferon, the percentage of cells with nuclear YAP is greatly reduced (blue nuclei, right panel). Image credit: Krupakar Subramaniam. Bottom: Model. Type III and Type I IFN receptor signaling activate LATS1 to curtail tissue repair during acute viral infection. Left-hand panel: During acute viral infection, high concentrations of Type III and/or Type I IFN receptor signaling trigger JAK-dependent, STAT1-independent phosphorylation of LATS1, leading to phosphorylation and degradation of YAP and reduced tissue repair activities mediated by YAP target genes. In rapidly proliferating cell types, active LATS1/2 also blocks repair in part via a p53-dependent mechanism. Right-hand panel: During resolution of viral infection, lower concentrations of Type III and/or Type I IFN may continue to activate STAT1-mediated antiviral defenses but no longer activate LATS1/2, allowing epithelial repair to resume.

#Interferons protect against #ViralInfection, but can hinder tissue repair - how? @ellenfoxman.bsky.social &co show that high IFN levels suppress #BronchialCell migration & proliferation during tissue repair via JAK-driven LATS1 activation, independent of STAT1 @plosbiology.org 🧪 plos.io/4k1pyKA

Nasal Cells Fight the Common Cold Via Interferons A rapid interferon response from nasal epithelial cells induces a cascade of responses during infection, from reduced viral load and cell damage to inflammation.

#Nasal cells fight the common #cold via #interferons ...

| #nose | #virus | #infection | #rhinovirus | #pathogen | #publichealth | By @lauraatran.bsky.social via the-scientist .com

It was an honour to speak at the first session ever on Nucleic Acid Sensing at the BSI congress. What a great meeting it was! I enjoyed meeting old and new friends & collaborators. Thanks for the invite! #BSI25 #interferons #InnateImmunity

#cytokines2025

Day 2 starts with a major symposium with Charlie Rice as the keynote! This session highlights my favorite cytokine -interferons!

#interferons #seattle #conference

Great honor to welcome Dr. Charles Dela Cruz, past @ats-pitb.bsky.social Chair, to @tulanemedicine.bsky.social today! He is giving an outstanding talk on COVID-19 and interferons—sharing deep insights into pathogenesis and host responses. #COVID19 #Interferons #ATS

#Medsky🧪 #IDsky #immunosky #publichealth Overview of the molecular & cellular mechanisms of IFN induction & signaling and of their pathophysiological roles.
#Interferons (IFNs) are a crucial family of signalling proteins that play vital roles in the immune system.

Interferons in health and disease The cytokine messenger proteins known as interferons are central to protective immune responses against infections, but they are also involved in inflammatory and autoimmune diseases. This review maps...

Molt bona revisió sobre el paper dels #Interferons tant en la salut com en la malaltia. www.cell.com/cell/fulltex...

#InterferonPower! Thrilled for our latest work @cp-cell.bsky.social! With @danielboehmer.bsky.social, we dug into tons of papers & created what we hope will be a go-to resource for immunologists & non-immunologist about type I, II, III (& IV😉) #interferons! Free👉 authors.elsevier.com/a/1leKGL7PXu...

HNMT Promotes the Occurrence and Progression of Nasopharyngeal Carcinoma by Inhibiting the IFN/TXNIP/p53 Axis - Current Medical Science Objective Histamine N-methyltransferase (HNMT) is involved primarily in histamine metabolism, but emerging evidence suggests its potential role in cancer progression. This study investigated the role ...

This study uncovers that #Histamine N-methyltransferase drives #nasopharyngeal #carcinoma by blocking Thioredoxin-interacting protein and p53, disrupting #interferons, revealing HNMT–IFN/TXNIP/p53 axis as a potent #therapeutic target. #medsky

Read: link.springer.com/article/10.1...

Second keynote by Ana Martín Villalba @dkfz.bsky.social on the role of #interferons in brain development and aging. Very fascinating topic in the total absence of viruses!
#IFNSymposiumHD

New immune mechanism discovered to protect the gut A research team from Canada, with the participation of Sebastian Weis’ group from the Leibniz-HKI and the Univer…

How does the gut stay healthy during worm infections? 🛡️🪱 A new Canadian-German study in #Cell shows #interferons help protect tissue. Not by killing worms, but by boosting gut resilience!

🗞️ News article: lmy.de/qMldA
💡Publication: lmy.de/wcghm

#DiseaseTolerance #InfectionBiology #LeibnizHKI

What a fantastic day spent UW Immunology! Lot of fun at my seminar, & amazing discussions about #interferons, host derived signals, #inflammasome, inflammatory diseases, & the many different ways cells can die & their consequences! Thanks @ramlabuw.bsky.social @drewoberst.bsky.social for hosting me!

Research Article

Correlation Between Interferon Response Gene Score and Disease Activity in Juvenile Dermatomyositis

📖 www.jrheum.org/cgi/content/...
@sickkidsto.bsky.social

#interferons #juveniledermatomyositis

Editorial

Interferon Response Gene Score in Juvenile Dermatomyositis

📖 doi.org/10.3899/jrhe...

#interferons #juveniledermatomyositis

IL-10 targets IRF transcription factors to suppress IFN and inflammatory response genes by epigenetic mechanisms - Nature Immunology Ivashkiv and colleagues show that IL-10 inhibits the expression and DNA binding of IRF1 and IRF5, two transcription factors that have an amplifying role in the induction of inflammatory NF-κB target g...

#EpigeneticPower! Ivashkiv, Mishra &co show @natimmunol.bsky.social that anti-inflammatory IL-10 epigenetically silence IRF1 & IRF5 gene transcription by decreasing H3K27ac & chromatin accessibility, thus preventing sustained #interferons & IL6/TNF signaling! www.nature.com/articles/s41...

#WeekendRead! #MysterySolved! Saidoube @casanovalab.bsky.social Gillet @ahmad-yatim.bsky.social &co show @jem.org that excessive TLR7 activation in pDCs drives type I #Interferons protecting against SARS-CoV-2 but at the same time causing chilblains!
rupress.org/jem/article/...

GM-CSF–mediated epithelial-immune cell cross-talk orchestrates pulmonary immunity to Aspergillus fumigatus During mold infection, epithelial-derived GM-CSF licenses neutrophil killing of fungal cells, leading to improved survival.

#WeekendRead! #EveryCellIsAnImmuneCell! Mills @fungalspore.bsky.social &co show @ Science Immunology that during lung fungal infections, lung epithelial cells independently respond to IL-1 & type III #interferons by producing GM-CSF which potentiates fungal killing by neutrophils!

Do you work on #interferons, come join the family!
go.bsky.app/71vKZJA

Current #immunology lab openings now on our lab website for how to apply as post doc or PhD student 🥳
sites.google.com/view/thesant...

Interest in #interferons is a requirement!

Just ignore the news area lol Many 2024 good news to update incl grants, studentships, talks, etc when I find time! 😀

2021 marked our @cp-cell.bsky.social paper on all types #interferons across the respiratory tract during #COVID_19, always with Benny & Achille & many other friends, we recently discussed also @cp-trendsimmuno.bsky.social (doi.org/10.1016/j.it...)! 6/ www.sciencedirect.com/science/arti...

IFN-λ suppresses intestinal inflammation by non-translational regulation of neutrophil function - Nature Immunology The effect of the cytokine IFN-λ in non-epithelial cells remains unclear. Zanoni and colleagues show that IFN-λ specifically activates a signaling pathway that diminishes the production of reactive ox...

The first paper form the lab with @achillebro.bsky.social was about the activity of type III #interferons (a great love ❤️ in the lab!) on #neutrophils during #colitis @natimmunol.bsky.social 2/ www.nature.com/articles/ni....

Type III interferons induce pyroptosis in gut epithelial cells and impair mucosal repair Intestinal damage following colitis or irradiation induces type III interferons (IFNs), which delay the healing of the intestinal epithelium. IFN-λ directs the sensing of Z-form nucleic acids generated during gut injury and repair, triggering cell death and altering healthy epithelial regeneration.

#EveryCellIsAnImmuneCell!💥Thrilled for the final version of our paper @cp-cell.bsky.social! We show that type III #interferons control ZBP1 activation driving gasdermin C cleavage & delaying gut repair by inducing #pyroptosis in intestinal epithelial cells! 1/n www.cell.com/cell/abstrac...

Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma caseation Sur Chowdhury et al. report that Mycobacterium tuberculosis (Mtb) infection results in the release of neutrophil extracellular traps (NETs) that promote Mtb replication and associate with tissue damage. Blocking NET release results in better control of Mtb replication, revealing a strategy for treating these deadly infections.

#WeekendRead! #ZombieNeutrophils! #InterferonsFriendsOrFoes?! Stallings &co show @ Cell Host & Microbe that micobacterium drives the releases of NET from live neutrophils (that lose their 🧠!) thanks to PAD4 & type I #interferons, favoring #Myb growth! www.cell.com/cell-host-mi...

Fantastic day @ Aarhus University talking cool science & discussing the power of #InnateImmunity (and a bit of #interferons 😉) in shaping the adaptive immune response!

In Paris to give a lecture on #interferons during antiviral immunity @sorbonne-universite.fr . If you think science is hard, try #teaching! 🧑‍🏫🧑‍🔬😱🧪

So thrilled to have our work @ Cell showcased @science.org! We show that type III #interferons determine gut repair in mouse models of intestinal damage & IBD patients! Open access link to the paper 👉👉👉 authors.elsevier.com/a/1k2OAL7PXq...