#PsACAREHub #PsoriaticArthritis #AutoimmuneResearch #Immunology #AcademicHiring #ScienceJobs #Rheumatology

📢 Help us spread the word! Like, share, and tag potential candidates who may be interested in joining the PsA CARE Hub. Together, we can drive innovation and improve outcomes for people living with PsA.

🔍 We're Hiring! We will soon be recruiting Associate and Assistant Research Scientists to join this groundbreaking initiative. If you're a scientist passionate about inflammation, immunology, or any field that can be applied to PsA research, stay tuned for opportunities!

focused on unraveling the cellular and molecular mechanisms driving PsA. By providing mentorship, cutting-edge resources, and a collaborative research environment, the Hub will empower the next generation of researchers to establish independent programs dedicated to PsA discovery.

PsA remains an underexplored disease at the mechanistic level, limiting the development of innovative treatments. The PsA CARE Hub, based at @YorkUniversity and funded by the @KrembilF, will address this critical gap by recruiting and supporting early-career scientists

Curious about the details? Check out the full paper here: www.sciencedirect.com/science/arti...
Big shoutout to our amazing team and BIG thanks to the funding agencies that supported this work! CIHR, Arthritis Society of Canada and Banting Research Foundation

Next steps? Targeting TRAF1/cIAP2 interaction with small molecules or biologics! Could this be the next generation of RA therapy? Let’s find out.

Unlike current RA therapies that block cytokines, our approach prevents inflammation at its source—without broad immune suppression. This could help patients who don’t respond to existing treatments!

✅ Protected against LPS-induced septic shock
✅ Significantly reduced joint inflammation & disease severity in an RA model

This suggests that disrupting TRAF1/cIAP2 signaling lowers inflammation without shutting down immunity!

🟩 The V203A mutation blocks TRAF1’s interaction with cIAP2.
🟩This shuts down TRAF1’s ability to amplify TLR4-driven inflammation.
🟩As a result, inflammatory cytokine production is significantly reduced.

We asked: Can we selectively disrupt TRAF1’s inflammatory function while keeping its protective role intact? Using CRISPR gene editing, we identified a mutation (V203A in humans, V196A in mice) that does just that!

TRAF1 is an immune signaling adapter linked to RA risk. It has a paradoxical role: it can both promote and suppress NF-κB & MAPK signaling. This complexity has made it hard to target therapeutically.

#RA is an autoimmune disease where chronic inflammation leads to joint damage. Current treatments target inflammatory cytokines, but many patients don’t respond or develop resistance. We need new approaches!

"reviewer 1" had a page and a half of comments 🙂

Deal!

Would be nice if made available on zoom 🙂

Congrats, Sunny! Great work