Ellen Foxman's Avatar

Ellen Foxman

@ellenfoxman.bsky.social

Associate Professor, Immunologist, Physician-Scientist. Studying human immunology, innate immunity, host-virus interactions for better diagnosis, treatment, prevention. Opinions are my own.

2,551 Followers  |  1,084 Following  |  47 Posts  |  Joined: 13.11.2024
Posts Following

Posts by Ellen Foxman (@ellenfoxman.bsky.social)

Once I saw a Harrier at dusk flying right past me β€”will never forget. Thank for sharing these photos!

06.02.2026 12:15 β€” πŸ‘ 2    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
Preview
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

Mechanistic insights into the impact of prenatal viral infections on maternal and offspring immunity

www.nature.com/articles/s44...

02.02.2026 13:51 β€” πŸ‘ 4    πŸ” 2    πŸ’¬ 0    πŸ“Œ 0
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.

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 πŸ§ͺ plos.io/4k1pyKA

28.01.2026 09:00 β€” πŸ‘ 4    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0
Preview
Β© CBC/Radio-Canada 2026. All rights reserved.

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-...

02.02.2026 15:10 β€” πŸ‘ 3    πŸ” 1    πŸ’¬ 0    πŸ“Œ 1

Excited to see this beautiful image of nasal #organoids featured as biomedical Image of the day by @cellpress.bsky.social πŸ™πŸ™πŸ™ See full paper @cellpressblue.bsky.social #respiratory #lungs #EpithelialMechanics #IdSky #MedSky #ImmunoSky

31.01.2026 15:55 β€” πŸ‘ 12    πŸ” 2    πŸ’¬ 0    πŸ“Œ 0
Preview
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...

#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/...

29.01.2026 15:43 β€” πŸ‘ 7    πŸ” 3    πŸ’¬ 0    πŸ“Œ 0
Preview
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/content/infe... #lungs #MedSky #IDsky #ImmunoSky

29.01.2026 15:33 β€” πŸ‘ 1    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0
Preview
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...

Frequent presymptomatic household transmission of influenza A but not influenza B virus

www.nature.com/articles/s44...

28.01.2026 14:07 β€” πŸ‘ 9    πŸ” 4    πŸ’¬ 0    πŸ“Œ 0
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.

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 πŸ§ͺ plos.io/4k1pyKA

27.01.2026 14:00 β€” πŸ‘ 6    πŸ” 3    πŸ’¬ 0    πŸ“Œ 0

#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 πŸ¦› pathway! journals.plos.org/plosbiology/... πŸ‘‡πŸ‘‡πŸ‘‡

27.01.2026 20:33 β€” πŸ‘ 6    πŸ” 5    πŸ’¬ 0    πŸ“Œ 0
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.

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 πŸ§ͺ plos.io/4k1pyKA

27.01.2026 17:30 β€” πŸ‘ 5    πŸ” 2    πŸ’¬ 0    πŸ“Œ 1

Link to original paper: www.cell.com/cell-press-b...

24.01.2026 20:58 β€” πŸ‘ 4    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0
Preview
Nose-in-a-dish: Scientists recreate common cold in culture Rhinoviruses really nose how to change cells...

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...

24.01.2026 20:58 β€” πŸ‘ 11    πŸ” 2    πŸ’¬ 1    πŸ“Œ 0

Fantastic work @ellenfoxman.bsky.social &co! If you block the #InterferonPower, Rhinovirus activates NFkB & NLRP1 #inflammasome leading to IL1b secretion & excessive mucus production!

22.01.2026 02:23 β€” πŸ‘ 4    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0
Preview
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...

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...

20.01.2026 21:23 β€” πŸ‘ 20    πŸ” 10    πŸ’¬ 1    πŸ“Œ 1
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

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

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

19.01.2026 16:00 β€” πŸ‘ 17    πŸ” 3    πŸ’¬ 2    πŸ“Œ 0
Post image

Happy Birthday Christy Turlington.

02.01.2026 23:29 β€” πŸ‘ 3    πŸ” 2    πŸ’¬ 1    πŸ“Œ 0
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.

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.

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

02.10.2025 17:11 β€” πŸ‘ 193    πŸ” 57    πŸ’¬ 7    πŸ“Œ 6
Preview
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 ...

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

09.10.2025 21:31 β€” πŸ‘ 33    πŸ” 17    πŸ’¬ 2    πŸ“Œ 1
Preview
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 …

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...

13.10.2025 15:26 β€” πŸ‘ 19    πŸ” 7    πŸ’¬ 0    πŸ“Œ 1
Preview
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...

#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...

23.06.2025 13:45 β€” πŸ‘ 9    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0
Regulations.gov

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

31.05.2025 13:47 β€” πŸ‘ 98    πŸ” 87    πŸ’¬ 6    πŸ“Œ 8
Preview
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...

Nice coverage of our H5 mRNA work by Jon LaPook tonight on @cbseveningnews.bsky.social

www.cbsnews.com/video/the-sc...

30.05.2025 01:45 β€” πŸ‘ 55    πŸ” 20    πŸ’¬ 0    πŸ“Œ 1
Flier for my talk Friday 5/30 at 7 p.m.

Flier for my talk Friday 5/30 at 7 p.m.

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. πŸ§ͺπŸ¦‘πŸŒŽ

28.05.2025 11:02 β€” πŸ‘ 479    πŸ” 222    πŸ’¬ 12    πŸ“Œ 26

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!

21.05.2025 00:15 β€” πŸ‘ 81    πŸ” 25    πŸ’¬ 1    πŸ“Œ 2
Post image

The Nile from the International Space Station:

18.05.2025 23:28 β€” πŸ‘ 6634    πŸ” 705    πŸ’¬ 109    πŸ“Œ 31
Post image

Once in a while. Good morning Blue Sky

19.05.2025 10:06 β€” πŸ‘ 15216    πŸ” 1387    πŸ’¬ 309    πŸ“Œ 77

Congratulations!

19.05.2025 21:06 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
Video thumbnail

Spectacular view of 100,000 people attending the #HandsOff march in NYC

05.04.2025 20:44 β€” πŸ‘ 78267    πŸ” 17583    πŸ’¬ 1375    πŸ“Œ 1370

Thrilled to share our @elife.bsky.social paper "Inflammasomes primarily restrict cytosolic Salmonella replication within human macrophages" by 1st author Dr. @marisaegan.bsky.social (@cambupenn.bsky.social alum, now faculty @swarthmorecollege.bsky.social)! elifesciences.org/articles/90107 🧡(1/n)

02.04.2025 13:02 β€” πŸ‘ 97    πŸ” 26    πŸ’¬ 10    πŸ“Œ 3