DC knockout leads to the low-level outcomes of TD and the adaptive immune signals such as I17 shown in Fig 10. The innate immune signals, e.g. Iα and I6, are reduced partially but still remain at a certain level. Upon deletion of Th1 there are no significant changes in the CS-induced TD and proinflammatory outcomes. This result is in agreement with clinical data for low Th1 population density , and mice experiments showing that CS induced significantly the production of Th17 rather than Th1 . Deletion of Th17 or CD8+T cells leads to a significant reduction of TD so that the progression of COPD is halted seen in Fig 10(A). However, the CS-induced proinflammatory signals such as Iα and I6 are reduced but still maintain at a relatively high level compared to those in silico experiment of M1 knockout. Different from the CD8+T deletion, the knockout of Th-17 leads to a reduction of I17 to the baseline, as shown in Fig 10(D). These results are in line with experiments in mice [70, 71].