lymphoid follicles [7].Furthermore, the significantly higher pulmonary Treg cell numbers in air-and CS-exposed CCR7 -/- mice correlated with a stronger abundance of lymphoid follicles, compared with WT animals (fig.1b and [7]).In contrast, baseline and chronic CS-induced Treg cell accumulation were severely compromised in lymph nodes of CCR7 -/- mice compared to WT controls (fig.1c).Our study provides evidence that CS exposure induces increased Treg cell numbers, first in the lung and secondly in the lymph node compartment.Whereas CCR7 is crucial for the homing of Treg cells to the lymph nodes, it is ultimately not required for the chronic CS-induced accumulation of these cells in the lung.However, we can not differentiate whether the observed CS-induced Treg increase results from the recruitment of natural Treg cells as opposed to the local induction of Treg cells from precursors.The methylation status of the FOXP3 promoter is generally considered to discriminate between natural and induced Treg cells.Further translational research is needed to elucidate the functional role of lymphoid follicles and Treg cells in the pathogenesis of COPD, for instance by determining the contribution of natural committed Treg cells versus induced Treg cells in pulmonary lymphoid follicles and lymph nodes.