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Posted On: 06/25/2021 4:13:14 AM
Post# of 148899
One thing I'm puzzled by is if the non-classical monocytes can carry viral fragments for up to 15 months then we should be seeing very early longhaulers who had the disease in March 2020 going into spontaneous remission.
He mentions CXCL4 (upregulator of VEGF) "which is a ligand of CCR5" I've never ran across that as a CCR5 ligand. However CXCL4 does bind to neuropilin-1 and leronlimab downregulates neuropilin-1.
He mentioned IFNy produced by Th1 (M1) cells. Leronlimab through macrophage differentiation decreases Th1 (M1) and increases Th2 (M2) cells. Notable is that reduction of IFN gamma would also downregulate CCR5.
One of the things I'd like to know, Dr. Patterson said they restored normal immune response but was that maintained after patients came off the drugs? Just got to that point in the video where that question was asked, apparently not yet.
ps. In my previous post antigens should actually be antibodies.
https://investorshangout.com/post/view?id=6167797
He mentions CXCL4 (upregulator of VEGF) "which is a ligand of CCR5" I've never ran across that as a CCR5 ligand. However CXCL4 does bind to neuropilin-1 and leronlimab downregulates neuropilin-1.
He mentioned IFNy produced by Th1 (M1) cells. Leronlimab through macrophage differentiation decreases Th1 (M1) and increases Th2 (M2) cells. Notable is that reduction of IFN gamma would also downregulate CCR5.
One of the things I'd like to know, Dr. Patterson said they restored normal immune response but was that maintained after patients came off the drugs? Just got to that point in the video where that question was asked, apparently not yet.
ps. In my previous post antigens should actually be antibodies.
https://investorshangout.com/post/view?id=6167797
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