Discover and read the best of Twitter Threads about #Inflammasomes
Most recents (3)
Very excited to share this work by the heroic team - @carolilucas Pat Wong @sneakyvirus @tiago21bio et al on “Longitudinal analyses reveal immunological misfiring in severe COVID-19”. A thread on our findings. #COVID19 #Pathogenesis (1/n)
nature.com/articles/s4158…
nature.com/articles/s4158…
In this study, we enrolled COVID+ patients and analyzed their immune responses and viral load over the course of their hospital stay. We also compared samples from COVID- healthy health care workers (HCWs) as comparison. (2/n) 
As reported by others, we found that COVID patients with severe disease have low T cell numbers and increased monocytes and neutrophils. We also found eosinophils come up in patients. This is bizarre 🧐 (3/n)
In some children, #COVID19 takes the form of #KawasakiDisease-like symptoms. So what exactly is #KawasakiDisease? It's an illness caused by inflammation of the blood vessels in children < 5 yrs of age. The exact cause is unknown but here's what we do know. Thread (1/n)
The #KawasakiDisease was first described in Japan by Dr. Tomisaku Kawasaki in 1967. Although more prevalent in Asians, it affects children of all ethnic groups. Symptoms include fever, red eyes, strawberry tongue, red rashes on the palms and soles. (2/n)
healthline.com/health/kawasak…
healthline.com/health/kawasak…
The #KawasakiDisease causes inflammation of the medium sized arteries, including the coronary arteries. If untreated, this can lead to serious conditions - heart disease, heart attack and death. (3/n)
ncbi.nlm.nih.gov/pubmed/25907703
ncbi.nlm.nih.gov/pubmed/25907703
Extremely exciting findings from @russellevance and @DBachovchin labs on NLRP1 activation following cleavage and degradation of N-terminal fragment now on biorxiv - biorxiv.org/content/early/… and biorxiv.org/content/early/… (1/9)
Destabilization of NLRP1b (e.g. cleavage by bacterial protease or degradation by bacterial ubiquitin ligase) releases non-covalently linked C-terminal fragment that can activate inflammasomes - caspase-1, pyroptosis, IL-1b, the works. (2/9)
Awesome mechanism for maintaining auto inhibition with associated fragments after auto-catalytic cleavage, and exploiting processive nature of the proteasome - using Nlrp1b as a “decoy sensor” sensing its own stability, a molecular "booby trap". (3/9)
