Fig. 1.

Studies from several laboratories are consistent with a model in which lung collectins minimize the inflammatory consequences associated with allergic airway disease by binding to allergens and antigens and regulating the functions of immune cells implicated in the pathogenesis of asthma (i.e. dendritic cells [DCs], T cells, and eosinophils [EOS]). Surfactant-associated protein D interacts with DCs to enhance the uptake and presentation of antigen, whereas SP-A affects the production of regulatory molecules (accessory molecules and cytokines) by DCs during allergen or antigen contact that can affect T-cell function. However, if the DCs remain in a less mature state in the lungs, migration may be inhibited to the lymph nodes, the site where DCs primarily present antigen to activate T cells. Concomitantly, in the lungs, SP-A and -D interact directly with T cells, preferentially T effector memory cells (TEMs), to inhibit proliferation and effector function. In addition, SP-D inhibits eosinophil chemotaxis and degranulation. We postulate that, during allergen challenge, SP-A and -D minimize the inflammatory responses that could damage the delicate alveolar epithelium. Thus, deficiencies or inactivation of surfactant proteins could contribute to the development of chronic inflammatory lung diseases. Modified from Wright.¹