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. 2022 Apr 25;13:883743. doi: 10.3389/fimmu.2022.883743

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Copyright © 2022 Serrano, Luque, Mitjavila, Blom, Rodríguez de Córdoba, Vega, Torras and Aran

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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PRP6-HO7 prevents pro-inflammatory surface TLR activation of Mo-DCs. Human Mo-DCs were incubated throughout their differentiation process with C4BP(β+), C4BP(β-) (both at 12 nM) and PRP6-HO7 (32 nM). DC maturation was achieved by TLR agonist treatment: Pam3CSK4 (TLR1/2), HKLM (TLR2), LPS-EK (TLR4), FLA-ST (TLR5), FSL-1 (TLR6/2). Cells were then collected, washed, and analyzed by flow cytometry for cell surface expression of CD83, CD86, CD80, CD40 and HLA-DR. MFI, median fluorescence intensity for the different surface markers. iDC, untreated, immature DCs; mDC, untreated, TLR-matured DCs. The results shown are the mean ± SD from 4-8 independent donors (*, p < 0.05; **, p < 0.01; ***, p < 0.001 compared with mDC).