TLR1 and TLR2 exploit distinct pathways following PAM3 stimulation.

(A–B) Sorted human blood pDCs were cultured during 4-hours with only medium (Ø) and with or without PAM3 in the presence or not of TLR1 neutralizing antibody (αTLR1 Ab), TLR2 neutralizing antibody (αTLR2 Ab), IgG1. FLU was used as control. (A–B) p38 MAPK (first panel), p65 NF-κB (second panel), AKT PI3K (third panel) at 3-hours. p38 MAPK (first panel), p65 NF-κB (second panel), AKT PI3K (third panel) at 3 different time points (2, 3, and 4 hours). Results include the mean of 8 independent donors. *p p p S1 Data. Ab, antibody; AKT, AKT serine/threonine kinase; FLU, influenza virus; IgG, Immunoglobulin G; MAPK, Mitogen-activated protein kinases; MFI, mean fluorescence intensity; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; PAM3, PAM3CSK4; pDC, Plasmacytoid predendritric cell; PI3K, Phosphoinositide 3-kinase; TLR, toll-like receptor.