Figure 1. Adaptive and innate immune responses in chronic respiratory disease.

a | Environm ental stimuli — suchas respiratory viruses, allergens and/or tobacco smoke — may act on genetically susceptible individuals to lead to an altered immune response, end-organ dysfunction and chronic inflammatory disease. b | An altered adaptive immune response involves antigen-presenting cells, primarily dendritic cells (DCs), that process and present antigens to memory B cells and T cells that drive the activation of effector immune cells (such as eosinophils and mast cells). Additional T cell subsets that regulate the adaptive immune response include T helper 17 (T_H17) cells, T_H9 cells and regulatory T cells (not shown). Alternatively, an altered innate immune response can involve airway epithelial cells (AECs) that activate innate immune cells, such as invariant natural killer T (iNKT) cells, M2 macrophages and innate lymphoid cells (ILCs). c | Effector cells or innate immune cells then produce type 2 cytokines — for example, interleukin-4 (IL-4) and IL-13 — that act on end-organ cells, especially AECs, to produce excess mucus, and on airway smooth muscle cells (ASMCs) to manifest airway hyperreactivity, which, to varying degrees, are both characteristic of patients with asthma and chronic obstructive pulmonary disease.