Finally, someone has solved a real problem with AI! No more having to take a paper in the format for a journal that rejected you, and reformat it for a new journal. Well done!!
https://t.co/J5HekY1Pc0
Part of my PhD work has been published!
We show that targeted IL-2 therapy, instead of worsening HLH, improves disease by inducing CD8⁺ T-cell exhaustion, an intrinsic immune brake that controls inflammation and redefines IL-2’s role in immunity.
https://t.co/euFtISFUPz
I don’t know why people complain so much about academia. Simply finish a PhD, apply 800 times, interview 300 times, finally know someone personally on the interview panel, and move to a country you’d never previously considered. Easy as that.
The feedback on this new episode has been something different! Many people are saying that this might be their favorite episode so far of the Night Science Podcast!
Writing a new review on #neuroimmunology and re-reading this paper from @Nature by @KevinJTraceyMD and colleagues. It was published in 2000, but it literally feels like a paper submitted today. So ahead of its time!
https://t.co/LlWhxLCE84
Neuroimmune crosstalk directs T cell differentiation for optimal viral clearance. With our collaborators, we show that neuropeptide CGRP produced by neurons during infection boosts Th1 differentiation while suppressing Th2, via RAMP3 on T cells. @Nature
https://t.co/wofhTDyZcX
Could inducing cell exhaustion be the solution to stop deadly hyperinflation?
We found that directing IL-2 to overstimulated CD8 T cells triggers exhaustion and prevents lethal inflammation!
#IL2#CD8Tcell#HLH
https://t.co/X8tlYxllAs
7) Reversing the exhaustion caused by NARA1 proved fatal. We concluded that exhaustion, usually considered to be reverted, can be beneficial in inflammatory contexts, and IL-2, typically a T-cell stimulant, may have the opposite effect in hyper-inflammatory conditions.