As we focus on the CS-induced immune response in the progression towards stable COPD in this work, other pathogenic mechanisms including exaggerated proteolytic activity, resulting from an imbalance between protease and antiprotease, and excessive oxidative stress from an oxidant-antioxidant imbalance  are implicitly involved, for example, in the representation of the M1→TD process as discussed above. Disruption of the balance between cell death and repair is also included indirectly in the TD component. These highly coarse-grained representations can be extended in more detail. Indeed, such studies have been undertaken recently in references [76–77]. However, the adaptive immunity has not been investigated and the insight into the cellular and molecular mechanisms of COPD is incomplete in these studies .