As asthma and allergic respiratory diseases have reached epidemic proportions over the last twenty years, research into the cellular and molecular pathogenesis of these disorders has exploded. Current paradigms emphasize the importance of a T lymphocyte–derived cytokine profile polarized toward type 2 molecules (Th2) that promote eosinophilic inffammation, such as interleukin (IL)-4,-5, and-13, rather than Th1 molecules such as IL-12 and interferon-(IFN-)(1).

A never-ending barrage of microbes, toxins, and antigens challenges the lung’s gas exchange function, making the respiratory epithelial surface an enormous battleground. The alveolar macrophage (mø)(AM) is the predominant immune effector cell resident in the alveolar spaces and conducting airways, and it is responsible for activating inffammatory responses sufficient to eliminate the interlopers (2, 3). However, an excessive inffammatory response might perturb gas exchange. This means that the AM must be “ambidextrous”—capable of both enhancing and suppressing inffammatory responses—and be “smart” enough to implement the effector program appropriate to the needs of the moment. Because this cell type is not only the most abundant but was among the first pulmonary immune cells to be extensively studied ex vivo, it is rather paradoxical that the AM is the forgotten cell in asthma. This conclusion is underscored by the fact that a recent exhaustive monograph on asthmatic airway inffammation has chapters on seven specific cell types, but none on AMs (4).