This presentation briefly summarizes the immunology and the pathology of the T cell cytokine interleukin-17A (IL-17A) in the lungs and addresses the potential of IL-17A as a pharmacotherapeutical target. Accumulating experimental and clinical evidence suggests that IL-17A is of importance for coordinating the adaptive and the innate components of pulmonary host defence in mammals. This evidence also suggests that IL-17 is produced by several subsets of T cells, including the T helper-17 (Th-17) subset. Until now, IL-17A has emerged mainly as an orchestrator of the local accumulation and activity of neutrophils; a role that IL-17A plays by inducing the release of C-X-C chemokines, colony-stimulating factors and IL-6. Even though its true role may be more diverse, the proposed role of IL-17A is relevant not only for pulmonary host defence against bacteria but also for inflammatory conditions in the lungs, such as severe asthma, chronic obstructive pulmonary disease, cystic fibrosis, and lung allograft rejection. From an immunological point-of-view, IL-17A's position at the interface of adaptive and innate immunity, is intriguing. It forwards the possibility that intervention targeting IL-17A can provide new therapy against inflammatory lung disorders related to poor endogenous control of local neutrophils.