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. 2017 Jul 13;8:796. doi: 10.3389/fimmu.2017.00796

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Copyright © 2017 Bisiaux, Boussier, Duffy, Quintana-Murci, Fontes and Albert.

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) or licensor 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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Toll-like receptor (TLR) and Dectin engagement by bacillus Calmette–Guérin (BCG) promotes NF-κB activation in an additive manner. (A–C) Data from Figures 4A–C and 5B were used to develop a mathematical model, querying whether TLR2&4 and Dectin-1&2 engagement is overlapping, additive, or synergistic in signaling via NF-κB. Cytokine concentrations were log-transformed, and ratio of remaining signal over BCG control condition was calculated for monocytes (A), neutrophils (B), and lymphocytes (C).