My bad .. misread that graph. Busy day. It doesn

My bad .. misread that graph. Busy day. It doesn't show percent occupied at all. I think it shows # of cells per uL staining with at least one CCR5 receptor bound to a fluorescent leronlimab. In other words these are the cells that have room for the fluoro labeled LL to bind. If they weren't free, then fluoroLL couldn't bind to label it. So there was a certain # of cells with at least one CCR5 receptor unbound (fluoroLL could bind). If baseline was 25 and after LL went down to 2, this would be 92% of cells that normally have a free CCR5 receptor that now are without at least one free CCR5 receptor available for the fluoroLL to go in and bind or mark. Or 92% of the amount of cells normally available for CCR5 signaling now have no CCR5 receptors free.

If this understanding is correct (big if!), then the older 2010 assay doesn't tell what percent of receptors are occupied, rather only the # of cells that have at least one/some free CCR5 unbound compared to how many normally have free CCR5. In the IV HIV paper, this percentage is 7%, or 93% less lymphocytes with at least one free CCR5.

I think the new RO assays are better, and measure something different, but obviously need to read some more.

Anyone else understand this RO business better?

I think for HIV and immunomodulation, we want to know what percent of lymphocytes we take out of business for having CCR5 available for HIV to bind and infect, or available to receive chemokine signaling to migrate.

The more lymphocytes of all types we can shut down CCR5 the better for HIV. For cancer we want more Tregs CCR5 shut down vs. CD8 killer Tcells, since we want Tregs to stay away for cancer. For reducing hyperinflammation and reducing autoimmunity, we want more Tregs I think. With different CCR5 densities, we can somehow effect which Tcells migrate more.

New InCellDX RO assays are good because measure RO on different T cell subtypes .. Tregs vs killer Tcells.

Maybe some day this will all make sense.