Ben Gern

@bengern.bsky.social

Pediatric Infectious Diseases physician-scientist at Seattle Children’s studying spatially-resolved immune responses during tuberculosis - (he/him) - gernlab.com

Pleased to see this out now in @jem.org 🔬 We characterise the early immune response during M. tuberculosis infection in mouse models and demonstrate a detrimental role for type I interferon activated neutrophils in TB lesions. Thanks to all involved @crick.ac.uk and i3S, Porto.

Journal of Experimental Medicine@jem.org · 12mo ago

William J. Branchett, Anne O’Garra @crick.ac.uk et al. reveal that type I signaling early during M. #tuberculosis infection favors #neutrophil swarming and limits CD4+ T cell–#macrophage interactions in #TB lesions, impeding TB disease control. rupress.org/jem/article/...

A nice discussion here of our work on the early immune response in M. tuberculosis infection and the great recent paper from @bengern.bsky.social et al

Journal of Experimental Medicine@jem.org · 11mo ago

First impressions count in #TB. Andrea Cooper @uniofleicester.bsky.social discusses studies by @wjbranchett.bsky.social et al. (rupress.org/jem/article/...) and @bengern.bsky.social et al. (rupress.org/jem/article/...), in Insights: rupress.org/jem/article/...

Asthma is a chronic disease characterized by acute, intermittent, recurrent episodes of airway inflammation. A decade of work developing the tools, techniques and collaborations needed to figure out how CD4+ T cells in the lungs propagate disease can be found here: www.biorxiv.org/content/10.1...

Tertiary lymphoid structures support the development of allergen-specific progenitor CD4+ T cells

Tissue-resident memory CD4+ T cells (TRM) are key sentinels of the adaptive immune response that provide a rapid, robust inflammatory response upon reactivation in non-lymphoid tissues. While CD4+ TRM...

biorxiv.org

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 Immunology@biorxiv-immuno.bsky.social · last yr.

NRF2 inhibition of alveolar macrophage MHC II expression during Mycobacterium tuberculosis infection https://www.biorxiv.org/content/10.1101/2025.08.16.670319v1

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

Happy to share a preprint from the Angelo lab many years in the making. Read on for a saga of multiplexed imaging, immunometabolism, and TB granulomas with some fun side quests into the realms of geographical information sciences and transcriptomics… (1/20) doi.org/10.1101/2025...

The immunometabolic topography of tuberculosis granulomas governs cellular organization and bacterial control

Despite being heavily infiltrated by immune cells, tuberculosis (TB) granulomas often subvert the host response to Mycobacterium tuberculosis (Mtb) infection and support bacterial persistence. We prev...

doi.org

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

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

biorxiv.org

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

biorxiv.org

Hello! I’m a Pediatric Infectious Diseases physician-scientist at Seattle Children’s. My lab studies spatially resolved host-pathogen interactions in order to understand how to better treat infection diseases, focusing on tuberculosis. I’m looking forward to building the scientific community here!

Bild