Ben Hale

In a new article with Kevin Groen, we review the most recent scientific developments relating to autoantibodies targeting type I interferons and their impacts on severe viral disease: doi.org/10.1016/j.covi…

📢 JEM is delighted to introduce the 2026 Associate Editors: Semir Beyaz (@beyazlab), Coco Chu (@CChu_89), Erin M. Gibson (@ErinMGibson), Benjamin G. Hale (@BenHalePhD), Guideng Li (@Guideng4), Esther Obeng, João Pereira, and Pamela Rosato. Welcome! 👉 hubs.la/Q03_03HM0

Groen, @benhalephd et al. @uzh__Virology identify interferon-λ #autoantibodies in 11.8% of those with #CysticFibrosis, a prevalence >10-fold higher than expected. In vitro & clinical analyses suggest the antibodies may impact mucosal pathology. hubs.la/Q03-pH_Z0

Type I interferon autoantibody footprints reveal neutralizing mechanisms and allow inhibitory decoy design. From Kevin Groen, Benjamin Hale @BenHalePhD and colleagues 👉 hubs.la/Q03Yb_kW0 📘 Part of 2025: The Year in Experimental Medicine hubs.la/Q03Yc1LV0

Thank-you @casanova_lab for the invitation to be a participant at your celebratory Novo Nordisk Prize Symposium. I appreciated being able to present alongside an array of leading researchers, & to meet many welcoming people in the field of Inborn Errors of Immunity! Congrats!

'TRIM28 is a target for paramyxovirus V proteins'. Work by Gauthier Lieber addresses whether host endogenous retroelements contribute to antiviral defence. As evidence, he describes a viral mechanism that might limit this response. @PLOSPathogens doi.org/10.1371/journa…

Now in press: Marie Lork et al studied host transposable elements during influenza A virus infection. We found evidence that some produce dsRNA, but that these host dsRNAs are limited from reaching the cytosol by the viral NS1 protein. @emboreports embopress.org/doi/full/10.10…

'TRIM28 is a target for paramyxovirus V proteins' - the major project from Gauthier Lieber while he was a PhD student in my lab is now available as a preprint: biorxiv.org/content/10.110…

@PizzornoAndres @LabWaggoner Thank-you!

@LabWaggoner @BenHalePhD Beautiful paper. Great job @BenHalePhD and collabs. !

An atlas of protein phosphorylation dynamics during interferon signaling @BenHalePhD pnas.org/doi/10.1073/pn…

Type I interferon autoantibody footprints reveal neutralizing mechanisms and allow inhibitory decoy design. New study from Kevin Groen, Benjamin Hale (@BenHalePhD) and colleagues @UZH_en: hubs.la/Q03cMv_Y0 #Autoimmunity #Immunodeficiency #InfectiousDisease

A superb study by @BenHalePhD : Type I interferon autoantibody footprints reveal neutralizing mechanisms and allow inhibitory decoy design rupress.org/jem/article/22…

@casanova_lab Thank-you!

An immune system defect makes affected individuals vulnerable to severe viral diseases such as influenza or COVID-19. It is caused by the body's own antibodies. UZH researchers have now generated “decoy molecules” that restore the immune defense – the foundation for a possible new therapy. news.uzh.ch/en/articles/me…

AutoAbs neutralizing IFN-Is exacerbate severe viral diseases. Groen et al. @BenHalePhD @UZH_en identify IFN-I regions commonly targeted by these autoAbs and develop a proof-of-concept decoy strategy to alleviate pathogenic effects. hubs.la/Q03cMHp90

.@SonjaFernbach, Mair, @BenHalePhD et al. dissect how rare anti-IFN-I autoantibodies develop and weaken defenses over time, making some individuals more susceptible to infections. hubs.la/Q02TJtPp0 📘 In our #Cytokines collection: hubs.la/Q02TJssf0 #cytokines2024

The Phenocopies of IEI session at #ESID2024 features experts Steve Holland, @anne_puel, @BenHalePhD, Aude Magerus, Sophie Hambleton, and @grvsadrian exploring how similar phenotypes emerge from different genetic causes. #IEI #ESID

.@SonjaFernbach, Mair, @BenHalePhD @UZH_Virology and colleagues dissect how rare anti-IFN-I autoantibodies develop and weaken defenses over time, making some individuals more susceptible to infections. hubs.la/Q02H58D10 #Autoimmunity #Immunodeficiency #InfectiousDisease

New work from @BenHalePhD (hubs.la/Q02H5Gdh0) shows that about two percent of the population develop autoantibodies against type 1 interferons, mostly later in life, making individuals more susceptible to viral diseases like #COVID19. From @UZH_en: hubs.la/Q02H5vYx0

By tracing development of anti-IFN-I autoantibodies in individuals over a 35 year period, @BenHalePhD et al suggest that loss of self-tolerance prior to immune-triggering poses a risk for lifelong autoantibody-mediated functional IFN-I deficiency. hubs.la/Q02H59Hq0