Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease

Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogenesis of COPD are unclear. Therefore, we investigated the roles of T and B lymphocytes and group 2 innate lymphoid cells (ILC2s) in airway inflammation and remodelling, and lung function in an experimental model of COPD using mice that specifically lack these cells (Rag1(−/−) and Rora(fl/fl)Il7r (Cre) [ILC2‐deficient] mice). Wild‐type (WT) C57BL/6 mice, Rag1 (−/−), and Rora(fl/fl)Il7r (Cre) mice were exposed to cigarette smoke (CS; 12 cigarettes twice a day, 5 days a week) for up to 12 weeks, and airway inflammation, airway remodelling (collagen deposition and alveolar enlargement), and lung function were assessed. WT, Rag1 (−/−), and ILC2‐deficient mice exposed to CS had similar levels of airway inflammation and impaired lung function. CS exposure increased small airway collagen deposition in WT mice. Rag1 (−/−) normal air‐ and CS‐exposed mice had significantly increased collagen deposition compared to similarly exposed WT mice, which was associated with increases in IL‐33, IL‐13, and ILC2 numbers. CS‐exposed Rora(fl/fl)Il7r (Cre) mice were protected from emphysema, but had increased IL‐33/IL‐13 expression and collagen deposition compared to WT CS‐exposed mice. T/B lymphocytes and ILC2s play roles in airway collagen deposition/fibrosis, but not inflammation, in experimental COPD.