I know that LL is a CCR5 blockade. In samples wit

I know that LL is a CCR5 blockade.

Quote:

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In samples without Leronlimab, we observed CCR5 internalization in response to MIP-1α, MIP-1β, and RANTES (Figure 1B). Following treatment with Leronlimab, we found increased frequencies of CCR5+CD4+ T cells where CCR5 was resistant to internalization following treatment with all three CCR5 ligands, indicating that Leronlimab both stabilized surface CCR5 expression and prevented its internalization. Thus, it is critical to account for this Leronlimab-induced increase in surface CCR5 levels for CCR5 RO measurements.

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I bolded the words "following".
The way I read this is:
They introduced RANTES and the other ligands of CCR5, MIP alpha and beta.
That internalized CCR5 and subsequently lowered expression of surface bound CCR5, however were appreciated internal to the cell.
Then they introduced LL which we know like a stronger magnet, can displace weaker ligands and replace them with itself.
After introducing LL, surface expression of CCR5 increased. Where did the CCR5 come from? From within the cell. Maybe LL did not enter the cell, but maybe LL pulled it back out to be expressed, thereby dislodging CCL5 and other ligands to bind to it.
This study indicates 100% RO after full dosing of LL.