I have read many places that leronlimab inhibits N
Post# of 154867
(Total Views: 663)
Posted On: 06/30/2021 10:51:03 PM
I have read many places that leronlimab inhibits NF-kB signaling and downregulates TNF-alpha
From one of your older posts ohm, I remember we also inhibit the mTOR pathway
I am not sure if there is therefore a connection to JNK?
Regardless, even if we just inhibit NF-kB and downregulate TNF-alpha, wouldn't we downregulate ICAM-1 expression? I have been reading up on ICAM-1 as it relates to monocyte adhesion and vascular inflammation but also ICAM-1 and many psychiatric disorders.
Here is a snippet from an article I was looking at
https://pubmed.ncbi.nlm.nih.gov/31398058/
If I am understanding correctly, this means that by decreasing ICAM-1 expression, we are basically making it so the CD16+ monocytes cannot attach to the endothelium as easily.
I think you may be suggesting that same thing by saying
but wanted to see if this was a different angle to view if from?
Thank you for the knowledge drop as always!
From one of your older posts ohm, I remember we also inhibit the mTOR pathway
Quote:
CCR5 blockade of CCL5 disrupts the mTOR/4E-BP1 pathway dysregulating elF4E. With elF4E disrupted the COVID-19 virus 5' -end cap it would be unable to separate it's mRNA and duplicate.
I am not sure if there is therefore a connection to JNK?
Regardless, even if we just inhibit NF-kB and downregulate TNF-alpha, wouldn't we downregulate ICAM-1 expression? I have been reading up on ICAM-1 as it relates to monocyte adhesion and vascular inflammation but also ICAM-1 and many psychiatric disorders.
Here is a snippet from an article I was looking at
https://pubmed.ncbi.nlm.nih.gov/31398058/
Quote:
Monocyte subsets have been associated with cardiovascular disease, yet it is unknown how different subsets are recruited to the endothelium. This study demonstrates the formation of distinct ICAM-1 N-glycoforms in the activated endothelium and reveals a key role for high mannose ICAM-1 in mediating proinflammatory CD16+ monocyte adhesion.
If I am understanding correctly, this means that by decreasing ICAM-1 expression, we are basically making it so the CD16+ monocytes cannot attach to the endothelium as easily.
I think you may be suggesting that same thing by saying
Quote:
TNF-a is also necessary for non-classical monocytes for endothelial cell adhesion.
but wanted to see if this was a different angle to view if from?
Thank you for the knowledge drop as always!
(4)
(0)