While animal studies support a role for DCs in COPD pathology,40–42 studies examining DC subsets by immunohistochemistry or flow cytometry in COPD have yielded inconsistent results.43 We found that aged pIgR−/− mice had increased moDC numbers and activation in the lungs as evidenced by increased pRelA, a marker of NF-κB activity.44 Reduction of the bacterial burden by antibiotic treatment blocked recruitment and activation of moDCs,26 indicating that airway bacteria are the primary stimulus for moDC differentiation in pIgR−/− mice. Here, NFKB1 is linked to chronic obstructive pulmonary disease.