Enteric Immunity Simulator (ENISI) output results and assessment of the role of the Peroxisome Proliferator Activated Receptor γ (PPARγ) in both the myeloid and T cell subset modulated T cell responses after <i>Helicobacter pylori</i> infection <i>in silico</i> in the gastric lamina propria (LP) and gastric lymph nodes (GLN).

<p>The <i>H. pylori</i> ABM was run as a time-course for 60 days. Model parameters were changed to simulate myeloid or T cell-specific PPARγ knockout systems as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0073365#pone.0073365.s007" target="_blank">Table S2</a>. Dynamical variation of Th1 (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0073365#pone-0073365-g006" target="_blank">Figure 6A, 6G</a>) as well as Th17 (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0073365#pone-0073365-g006" target="_blank">Figure 6B, 6H</a>) and regulatory T cells (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0073365#pone-0073365-g006" target="_blank">Figure 6C, 6I</a>) changing over time were plotted. A functional T-test was used with 95% confidence interval to create statistics assessing differences in the myeloid and T cell specific PPARγ knock-out for Th1 (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0073365#pone-0073365-g006" target="_blank">Figure 6D, 6J</a>), Th17 (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0073365#pone-0073365-g006" target="_blank">Figure 6E, 6K</a>) and Treg (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0073365#pone-0073365-g006" target="_blank">Figure 6F, 6L</a>). A threshold value representing the critical value of significance vertically divides the plot into two parts, showing significant differences above the threshold. Data were obtained in 15 runs of the simulation for each different genotype.