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. 2021 Nov 19;12:794638. doi: 10.3389/fimmu.2021.794638

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Copyright © 2021 Chang, Wu, Webb, Tiwary, Hughes, Reed, Hwang, Waytashek, Boyle, Pessoa, Sylwester, Morrow, Belica, Fischer, Kelly, Pourhassan, Bochart, Smedley, Recknor, Hansen and Sacha

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Leronlimab increases cell surface CCR5 expression that is resistant to internalization. PBMC from humans (n=2; triangles) and rhesus macaques (n=2; circles) were incubated without (left, red) or with (right, blue) 5 μg/mL Leronlimab for 30 minutes at 37°C, then with either no treatment or 50nM of one the following CCR5 ligands: MIP-1α, MIP-1β, or RANTES, for an additional 30 minutes. After incubation, cells were stained for CCR5 (clone 3A9) and CD3, CD4, and CD8 surface markers. Cells were gated within live, CD3+, CD4+/CD8-, singlet populations. (A) Representative flow plots. (B) Graphs show normalized frequencies of CCR5+ of CD4+ T cells to frequency observed with untreated cells (no Leronlimab, no CCR5 ligands) from the respective donor.