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Of the therapeutic options developed against viral infections, clinical grade recombinant type I IFNs, (IFN-α/β) or type III IFNs (IFN-λ) raised much hope and interest among researchers. IFN-λ is particularly relevant as a gatekeeper of mucosal immunity: as we recently reported, it is able to induce an antiviral state, and simultaneously limits inflammation-driven tissue damage (The Journal of Experimental Medicine, 2020). Although IFN-λ’s acute antiviral activity is well-recognized, if and how prolonged exposure to this IFN might change the physiology of the lung remained largely overlooked. We demonstrated that, in a mouse model that mimics prolonged viral infection, IFN-λ decreases the effectiveness of the lung barrier, and predisposes to a lethal secondary infection with the Gram-positive bacterium Staphylococcus aureus (Science, 2020). Our findings give a potent mandate for rethinking the pathophysiological role of IFN-λ, and for avoiding its use in the most severe COVID-19 cases, which often develop superinfections.

Currently, we are further investigating how IFN-λ modifies the immune response elicited in the lung during viral and bacterial infections. By using traditional immunological techniques and cutting-edge omics approaches -such as single cell RNAseq and single cell proteomics- we will unravel how acute and prolonged exposure to microbial stimuli shapes the cellular and molecular landscape of the lung.

ZanoniLab

Histology of the lung of a mouse. Credit to Dr. Broggi

Division of Immunology

Division of Gastroenterology

Boston Children’s Hospital

The Karp Family Research Building 10.217

One Blackfan Circle, Boston, MA 02115

ZanoniLab

Unraveling inflammatory networks in health and disease

© 2022 Zanoni Lab

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