Ben Gern
@bengern.bsky.social
3.1K followers 460 following 8 posts
Pediatric Infectious Diseases physician-scientist at Seattle Children’s studying spatially-resolved immune responses during tuberculosis - (he/him) - gernlab.com
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bengern.bsky.social
I’m excited to announce that our paper, describing early and opposing roles for neutrophils and CD4 T cells in determining #TB lesion structure, is out at @jem.org ! Huge thanks to my lab, and the Urdahl, @michael-gerner.bsky.social, and Aitchison labs who made this possible

doi.org/10.1084/jem....
Reposted by Ben Gern
tomscriba.bsky.social
We are inviting applications for postdoctoral fellows in immunology of TB at the South African Tuberculosis Vaccine Initiative, University of Cape Town. For more information see the attached ad:

idm.uct.ac.za/media/739223
Reposted by Ben Gern
jem.org
Our October issue is here! rupress.org/jem/issue/22...
The cover image shows the lung of a mouse infected with M. #tuberculosis stained for #neutrophils (orange) normal lung parenchyma (blue), collagen (white) and CD4 T cells (green). See @bengern.bsky.social et al. rupress.org/jem/article/...
Reposted by Ben Gern
scienceinseattle.com
A recent study from the Gerner and Urdahl labs at UW and @seattlechildrens.org uncovers fundamental determinants of tuberculosis lung pathology. This has important implications for new strategies to prevent or treat tuberculosis.

🧐 See the abstract in @jem.org : https://bit.ly/41IdeHA
Reposted by Ben Gern
bpodaily.bsky.social
Conflict between the innate & adaptive immune system responses determines the kind of damage lungs suffer when infected with TB

Image made with @leicamicrosystems.bsky.social microscopy

📷 @bengern.bsky.social et al @seattlechildrens.org in @jem.org

➡️ bpod.org.uk/archive/2025...
Reposted by Ben Gern
alissarothchild.bsky.social
Happy to share our new pre-print, led by PhD student Linh Pham! We examine inhibition of MHC II expression by NRF2 during Mtb infection and its impact on innate-adaptive crosstalk. Special thanks to the Behar lab who helped us set up a T cell co-culture system for the project! #TB #immunology
biorxiv-immuno.bsky.social
NRF2 inhibition of alveolar macrophage MHC II expression during Mycobacterium tuberculosis infection https://www.biorxiv.org/content/10.1101/2025.08.16.670319v1
Reposted by Ben Gern
joanneflynn19.bsky.social
We are hiring! The Dept of Microbiology and Molecular Genetics is looking for faculty at the Assistant or Associate professor level (tenure track). Please consider joining our vibrant microbiology and immunology community at the University of Pittsburgh School of medicine
Reposted by Ben Gern
jem.org
#WomenInSTEM becoming independent: People should feel free to be themselves and do great science. We asked ten women researchers about their science and the process of setting up a lab as an independent researcher: rupress.org/jem/article/...
Reposted by Ben Gern
jem.org
Early and opposing #neutrophil and CD4 T cell responses shape pulmonary #tuberculosis pathology, say Benjamin Gern @bengern.bsky.social, Michael Gerner, Kevin Urdahl et al. rupress.org/jem/article/...

#TB
Reposted by Ben Gern
rupress.org
In @jem.org, @bengern.bsky.social et al. show that the early interplay between #neutrophils & CD4 T cells is pivotal in determining #TB pathology, and that depleting neutrophils can improve outcomes even at late timepoints, which has therapeutic relevance rupress.org/jem/article/...
Reposted by Ben Gern
jem.org
@bengern.bsky.social et al. show that the early interplay between #neutrophils & CD4 T cells is pivotal in determining #TB pathology, and that depleting neutrophils can improve outcomes even at late timepoints, which has therapeutic relevance rupress.org/jem/article/...
bengern.bsky.social
I’m excited to announce that our paper, describing early and opposing roles for neutrophils and CD4 T cells in determining #TB lesion structure, is out at @jem.org ! Huge thanks to my lab, and the Urdahl, @michael-gerner.bsky.social, and Aitchison labs who made this possible

doi.org/10.1084/jem....
Reposted by Ben Gern
gpollara.bsky.social
Tuberculosis continues to impair quality of life long after the antibiotics have finished...

Need to work out how to prevent and treat these post-TB sequelae.
#IDSky #TBSky
atsblueeditor.bsky.social
Contribution of Posttuberculosis Sequelae to Life-Years Lost from Tuberculosis Disease in the United States, 2015–2019

@atscommunity.bsky.social

www.atsjournals.org/doi/full/10....
Reposted by Ben Gern
bengern.bsky.social
Congrats on a really cool story, Erin!
Reposted by Ben Gern
mayerbarber.bsky.social
Best #Nikolaus 🎅! Our paper on how the 🫁 microenvironment can shape #innate immunity against #viruses is out @sciimmunology.bsky.social This was a herculean effort brilliantly led by @pauljbaker.bsky.social who singlehandedly established the model in the lab during the pandemic. 🧪 #Immunosky 1/9
Graphical summary of our paper.  In mice, prior lower airway exposure to diverse inflammatory stimuli, including chronic bacterial infections such as M. tuberculosis, acute bacterial infections such as pulmonary S. aureus, viral infections such as Influenza A, type-II allergic responses such as the OVA-Alum model, activation of pulmonary TLR9 by CpG or pulmonary TLR1/2 by Pam3CSK4
 leads to reduced viral burden upon subsequent infection with SARS-CoV-2 (SCV2). (2) This SCV2 restriction occurs prior to induction of SCV2-specific adaptive immune responses 
and is mediated through innate immune responses, including the induction of IFN-I, TNFα and IL-1 and sustained changes to the TRM (Tissue resident macrophage) cellular 
compartment and the pulmonary epithelium. (3) Innate cytokine and TLR signaling to both recruited immune cells and the pulmonary epithelium creates a microenvironment in the 
lung that limits early replication of SCV2. IFN-I signaling to pulmonary ECs (epithelial cells) increases expression of interferon-stimulated genes, that likely cell-intrinsically limit viral
 replication. TNF- or IL-1 suppress SCV2 independently of IFN-I signaling. TNF acts exclusively through radio-resistant cell types such as the lung epithelium, whereas IL-1 affords 
control both direct and indirectly, through either stromal and hematopoietic cell types, to restrict overall early SCV2 burden.
Reposted by Ben Gern
johngreensbluesky.bsky.social
My new book, Everything Is Tuberculosis, explores the history of our deadliest infectious disease. It's also about our horrifying present: TB still kills kills over a million people per year, even though it's been curable since the 1950s.

Signed copies can be ordered at everythingistb.com
yellow book cover reading Everything Is Tuberculosis: The History and Persistence of Our Deadliest Infection Signed Edition
Reposted by Ben Gern
mcsinton.bsky.social
Ok, in time for the International Day of Pride in STEM, here's a starter pack of LGBTQ+ immunologists. Since not everyone is open (or able to be open) about their identities, we're only adding people by request, so let me know if you'd like to be added #Immunosky #PrideInSTEM 🏳️‍🌈🏳️‍⚧️ go.bsky.app/7WTavcd
bengern.bsky.social
Hi! Would you include me in the global health starter pack?

I’m a PI focusing on #tuberculosis immunology at the Seattle Children’s Center for Global Infectious Disease Research and a peds ID specialist.
bengern.bsky.social
We are hiring a technician! This position is a great fit for motivated individuals who plan on going to graduate/medical school and want to study host-pathogen interactions using advanced imaging and immunologic tools. Please spread the word!

seattlechildrens.wd5.myworkdayjobs.com/External/job...
Reposted by Ben Gern
alissarothchild.bsky.social
So happy to share the latest preprint from our lab, led by grad student @PameliaLim9! Pamelia set out to study alveolar #macrophage innate sensing and found that lack of c-Maf and IL-10 enables Type I IFNs to enhance responses to low-dose LPS. www.biorxiv.org/content/10.1...
Absence of c-Maf and IL-10 enables Type I IFN enhancement of innate responses to low-dose LPS in alveolar macrophages
bioRxiv - the preprint server for biology, operated by Cold Spring Harbor Laboratory, a research and educational institution
www.biorxiv.org
bengern.bsky.social
I’m excited to share that this collaborative effort with Kevin Urdahl, Michael Gerner, and many others is out!

We show that preexisting immunity-driven CD4 T cells and neutrophils are opposing forces in determining tuberculosis lesion structure and pathogenesis.

#tuberculosis
CD4-mediated immunity shapes neutrophil-driven tuberculous pathology
bioRxiv - the preprint server for biology, operated by Cold Spring Harbor Laboratory, a research and educational institution
www.biorxiv.org