Ruth Franklin

So exciting to see this out!! More cool biology sure to come!! 🤩👀

No worries at all, next time!

Had a fantastic visit @roswellpark.bsky.social for the Post-Doctoral Symposium!! So many inspiring scientists doing cool work! Grateful for the invitation!

Can’t wait to read this!! Sure to be a fantastic resource! #InterferonPower

Super cool work, Ryan et al!!

Thanks, Xu!!

Regulation of inflammatory responses by pH-dependent transcriptional condensates Inflammation is an essential defense response but operates at the cost of normal tissue functions. Whether and how the negative impact of inflammation…

Exciting week! Congrats to @xuzhoulab.bsky.social, Ruslan Medzhitov, & coauthors on discovering a new mechanism to regulate inflammation!! 🎉 www.sciencedirect.com/science/arti...

Thanks so much!

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage Tissue repair programs must function alongside antiviral immunity to restore the lung epithelial barrier following infection. We found that macrophage-derived oncostatin M (OSM) counteracted the patho...

#WeekendRead! #InterferonsFriendsOrFoes?! @ruthfranklinlab.bsky.social, Medzhitov, Hoagland, Rodriguez-Morales &co show @science.org that macrophage-derived oncostatin M overcomes type I IFN detrimental responses during severe influenza lung infection by driving AT-II epithelial cell proliferation!

Thank you!!

Thank you!!

Thank you!

Thanks so much, Mohamed!

Thanks, Megan!

Thanks!!

Thank you!

Thanks, Igor! We’re super excited!

Thank you!

Thank you, Sunny!!

Thank you!

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage Tissue repair programs must function alongside antiviral immunity to restore the lung epithelial barrier following infection. We found that macrophage-derived oncostatin M (OSM) counteracted the patho...

I’m so proud to have been able to contribute to this story! Check it out for a cool tale about tissue repair under inflammatory conditions! Congrats @daisyah.bsky.social and @ruthfranklinlab.bsky.social on putting out the lab’s first paper 🫁🐁🦠

www.science.org/doi/10.1126/...

Thanks, Ryan!

Thank you!!

This project first started during my postdoc w/ Ruslan Medzhitov and I’m extremely grateful for his support! And finally, thank you to the reviewers, @sarahhross.bsky.social & the team @science.org, we’re thrilled to see this story in print! 9/fin

A huge thank you to the incredible members of my lab who made it all happen, especially @daisyah.bsky.social & Patricia, and all the coauthors for their contributions along the way! 8/n

tldr: Macrophage-derived OSM enables lung repair during inflammation. This opens the door to therapies that stimulate repair without compromising antiviral responses. 7/n

We also found an intriguing role for OSM in maintaining the transcriptional states of ATIIs, an area with many open questions! 6/n

We first thought that OSM was directly suppressing IFN-I, but with more digging (& insightful reviewer comments!), we discovered that OSM promotes ATII epithelial cell proliferation in the context of IFN-I --> a new mechanism of disease tolerance during infection and tissue damage! 5/n

Cue the macrophages! We focused on a cytokine they produce: OSM. Linked to inflammatory diseases, the role of OSM during steady state & acute infection was unclear. To our surprise, in response to flu or viral mimic, we found increased IFN-I and decreased host survival in the absence of OSM. 4/n

IFN-I is a key antiviral mediator, but also leads to immunopathology, including epithelial cell death and antiproliferative effects. Despite this, lungs undergo rapid repair after infection, suggesting a mechanism that drives proliferation in the context of IFN-I and tissue damage. 3/n