Ellen Foxman
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ellenfoxman.bsky.social
Ellen Foxman
@ellenfoxman.bsky.social
2.6K followers 1.1K following 47 posts
Associate Professor, Immunologist, Physician-Scientist. Studying human immunology, innate immunity, host-virus interactions for better diagnosis, treatment, prevention. Opinions are my own.
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Reposted by Ellen Foxman
Mechanistic insights into the impact of prenatal viral infections on maternal and offspring immunity

www.nature.com/articles/s44...
Mechanistic insights into the impact of prenatal viral infections on maternal and offspring immunity - npj Viruses
npj Viruses - Mechanistic insights into the impact of prenatal viral infections on maternal and offspring immunity
www.nature.com
February 2, 2026 at 1:51 PM
Reposted by Ellen Foxman
plosbiology.org
#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.
January 28, 2026 at 9:00 AM
ellenfoxman.bsky.social
Thank you to Bob McDonald for hosting me on @CBCRadioCanada to discuss our work @yaleschoolofmed.bsky.social on what leads to variation in common cold virus infections and how we tackled this using nasal organoids. Listen here: www.cbc.ca/listen/live-...
© CBC/Radio-Canada 2026. All rights reserved.
www.cbc.ca
February 2, 2026 at 3:10 PM
ellenfoxman.bsky.social
Excited to see this beautiful image of nasal #organoids featured as biomedical Image of the day by @cellpress.bsky.social 🙏🙏🙏 See full paper @cellpressblue.bsky.social #respiratory #lungs #EpithelialMechanics #IdSky #MedSky #ImmunoSky
bpodaily.bsky.social Biomedical Picture of the Day BPoD @bpodaily.bsky.social · 18d
Response to rhinovirus depends on levels of interferon production & viral load – differences revealed using a nasal organoid
📷 Julien Amat & Bao Wang, relating to B.Wang et al article
@yaleschoolofmed.bsky.social in @cellpressblue.bsky.social
➡️ bpod.org.uk/archive/2026... with
@rooph.bsky.social
January 31, 2026 at 3:55 PM
ellenfoxman.bsky.social
#Epithelialmechanics fans...interferons protect against viruses but also impair recovery post-infection. In new work @plosbiology.org we show that interferons block epithelial repair by co-opting the Hippo pathway #innateimmunity #lungs #respiratory journals.plos.org/plosbiology/...
Dose-dependent activation of the Hippo pathway by Type I and Type III interferons suppresses tissue repair by human bronchial epithelial cells
Interferons (IFNs) initiate antiviral defence when infected cells sense a virus protecting against infection via JAK/STAT signaling, but can hinder recovery by impairing tissue repair by an unknown me...
journals.plos.org
January 29, 2026 at 3:43 PM
ellenfoxman.bsky.social
www.thedoctorwillseeyounow.com/content/infe... #lungs #MedSky #IDsky #ImmunoSky
How Your Body Fights Off the Cold Virus
Ever wonder why some people get really bad colds and others never get sick? Modeling the cells in human noses and lungs suggests an answer.
www.thedoctorwillseeyounow.com
January 29, 2026 at 3:33 PM
Reposted by Ellen Foxman
Frequent presymptomatic household transmission of influenza A but not influenza B virus

www.nature.com/articles/s44...
Frequent presymptomatic household transmission of influenza A but not influenza B virus - Nature Health
Based on two waves of data collection from 748 households in Hong Kong, this analysis sheds light on the number of transmission events that occurred before manifestation of symptoms in influenza A and...
www.nature.com
January 28, 2026 at 2:07 PM
Reposted by Ellen Foxman
plosbiology.org
#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.
January 27, 2026 at 2:00 PM
Reposted by Ellen Foxman
lozanzi.bsky.social
#InterferonFriendsOrFoes? Another cool one @ellenfoxman.bsky.social &friends out @plosbiology.org about how excessive #IFNs delay repair by activating LATS & degrading YAP/TAZ in the Hippo 🦛 pathway! journals.plos.org/plosbiology/... 👇👇👇
January 27, 2026 at 8:33 PM
Reposted by Ellen Foxman
plosbiology.org
#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.
January 27, 2026 at 5:30 PM
ellenfoxman.bsky.social
Interested in the common cold virus? Check out this clip from the Naked Scientist podcast about our recent study in which we observed thousands of nasal cells interact to cause (or stop) symptoms of common cold infections. #MedSky #IDsky #lungs www.thenakedscientists.com/articles/int...
Nose-in-a-dish: Scientists recreate common cold in culture
Rhinoviruses really nose how to change cells...
www.thenakedscientists.com
January 24, 2026 at 8:58 PM
Reposted by Ellen Foxman
lozanzi.bsky.social
Fantastic work @ellenfoxman.bsky.social &co! If you block the #InterferonPower, Rhinovirus activates NFkB & NLRP1 #inflammasome leading to IL1b secretion & excessive mucus production!
ellenfoxman.bsky.social Ellen Foxman @ellenfoxman.bsky.social · 29d
Rhinoviruses cause common cold & asthma attacks but are also often benign. Using nasal organoids, we learned how the community of cells in the lining the nasal passages coordinates to respond to rhinovirus and which responses lead to excess mucus & inflammation. www.cell.com/cell-press-b...
Rhinovirus triggers distinct host responses through differential engagement of epithelial innate immune signaling
Rhinoviruses are the most frequent cause of common colds and also a major cause of respiratory distress in high-risk groups. Using single-cell sequencing of rhinovirus-infected nasal epithelial organo...
www.cell.com
January 22, 2026 at 2:23 AM
ellenfoxman.bsky.social
Rhinoviruses cause common cold & asthma attacks but are also often benign. Using nasal organoids, we learned how the community of cells in the lining the nasal passages coordinates to respond to rhinovirus and which responses lead to excess mucus & inflammation. www.cell.com/cell-press-b...
Rhinovirus triggers distinct host responses through differential engagement of epithelial innate immune signaling
Rhinoviruses are the most frequent cause of common colds and also a major cause of respiratory distress in high-risk groups. Using single-cell sequencing of rhinovirus-infected nasal epithelial organo...
www.cell.com
January 20, 2026 at 9:23 PM
Reposted by Ellen Foxman
cellpress.bsky.social
Cells in our nasal passages can detect common cold viruses and mount a defense before we catch it. spkl.io/63321Ao5fV

@ellenfoxman.bsky.social & colleagues
@cellpressblue.bsky.social
Rhinoviruses are the most frequent cause of common colds but also a major cause of respiratory distress in high-risk groups. Using single-cell sequen cing of rhinovirus-i nfected nasal epithelial organoids, Foxman and colleagues elucidate effective and maladaptive innate immune responses to rhinovirus infection and define targets for intervention
January 19, 2026 at 4:00 PM
Reposted by Ellen Foxman
copddoc.bsky.social
Happy Birthday Christy Turlington.
January 2, 2026 at 11:29 PM
Reposted by Ellen Foxman
greenrat.bsky.social
Neat trick if you polycolonal ab's suck. Incubate them with fixed cells with a KO of your protein of interest, then spin. Protocol here: www.med.upenn.edu/markslab/ass...
I was amazed how well it worked on first try (I'm sure that I can completely eliminate unspecific bands)
#WesternBlot #cellsky
On the left - western blot of B16F10 cells wt and KO for CDK8. Our in house produced antibodies give a lot of unspecific bands. On the right same probes with antibodies preincubated with fixed CDK8 KO cells - there is a specific band and faint unspecific bands, which can be probably eliminated with increase of amount of KO cells.
October 2, 2025 at 5:11 PM
Reposted by Ellen Foxman
marcveld.bsky.social
A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging

Naked mole rats get much older than closely related mamals of a similar size. cGAS mutations may have an important role in this.

www.science.org/doi/...
1/9
A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging
Efficient DNA repair might make possible the longevity of naked mole-rats. However, whether they have distinctive mechanisms to optimize functions of DNA repair suppressors is unclear. We find that naked mole-rat cyclic guanosine monophosphate–adenosine ...
www.science.org
October 9, 2025 at 9:31 PM
ellenfoxman.bsky.social
Happy to share this review just out in Current Opinion in Immunology on innate immunity in the respiratory tract - also check out the other reviews in this collection on Intrinsic Immunity edited by John MacMicking #ImmunoSky #IDSky #pulmsky #MedSky www.sciencedirect.com/science/arti...
Layers of defense: protection from respiratory viruses by epithelial-intrinsic immunity
A central challenge in defending mucosal barriers is protecting against pathogens while also limiting excessive inflammation. Respiratory viruses are …
www.sciencedirect.com
October 13, 2025 at 3:26 PM
ellenfoxman.bsky.social
#COVID19 revealed the urgent need for better ways to screen for & rule out respiratory virus infection. We present a nasal biomarker screening strategy to prevent & manage outbreaks @eBiomedicine.bsky.social #IDSky #MedSky #lungs @yaleschoolofmed.bsky.social www.thelancet.com/journals/ebi...
Nasal biomarker testing to rule out viral respiratory infection and triage samples: a test performance study
These results demonstrate the utility of a nasopharyngeal biomarker to rule out respiratory infection, with potential applications in outbreak management and/or routine screening in high-risk settings...
www.thelancet.com
June 23, 2025 at 1:46 PM
Reposted by Ellen Foxman
jeremymberg.bsky.social
ASSIGNMENT: COMMENT ON SCHEDULE F

1 week left to comment about Schedule F, potentially making NIH institute and center director essentially political appointees.

www.regulations.gov/commenton/OP...

1/n
Regulations.gov
www.regulations.gov
May 31, 2025 at 1:48 PM
Reposted by Ellen Foxman
scottehensley.bsky.social
Nice coverage of our H5 mRNA work by Jon LaPook tonight on @cbseveningnews.bsky.social

www.cbsnews.com/video/the-sc...
The scientists aiming to stay ahead of bird flu on dairy farms and prevent a human pandemic
So far, the only people to come down with bird flu got it from animals. Dr. Jon LaPook reports on how research is underway to keep bird flu from mutating into a form that could spread from person to p...
www.cbsnews.com
May 30, 2025 at 1:45 AM
Reposted by Ellen Foxman
whysharksmatter.bsky.social
Are you a scientist and not sure what to do to help with all the awfulness all around us? Inspired by Vietnam era activism, @standupforscience.bsky.social is hosting a series of "teach ins," in which scientists share a bit about their area of expertise and why it's important with the public. 🧪🦑🌎
Flier for my talk Friday 5/30 at 7 p.m.
May 28, 2025 at 11:02 AM
Reposted by Ellen Foxman
scottehensley.bsky.social
Check out this news story that @nature.com wrote describing our recent preprint where we tested our H5 mRNA vaccine in calves.

The data look good and we are currently testing the vaccine in lactating cattle...more to come!
nature.com Nature @nature.com · May 20
As bird flu sweeps across US poultry and cattle farms, researchers are racing to find ways to contain the outbreaks before they ignite a human pandemic. Now, a team of scientists has developed a fresh approach: the first mRNA bird-flu vaccine for cattle.

https://go.nature.com/4kbOvTe
Bird flu vaccine for cattle aces early test
Vaccines for livestock could reduce the risk of human outbreaks, but hurdles remain.
go.nature.com
May 21, 2025 at 12:15 AM
Reposted by Ellen Foxman
caroleeena.bsky.social
The Nile from the International Space Station:
May 18, 2025 at 11:28 PM
Reposted by Ellen Foxman
jonathanslater.bsky.social
Once in a while. Good morning Blue Sky
May 19, 2025 at 10:06 AM