Naive CD4 cells are capable of integrating signals from antigen-activated cells of the innate immune system and differentiating into effector CD4 cells, also termed T helper (Th) cells. According to the traditional paradigm explaining adaptive CD4 cell responses, there are two subsets of Th cells: the Th-1 and Th-2 subset. Each of these subsets undergoes a distinct differentiation pathway (a pathway that is characterized by a unique profile of cytokine production and has specific immunoregulatory functions). However, recent studies in mouse models have forwarded evidence of a third subset of Th cells: the Th-17 subset. As indicated predominantly in studies on mice, the Th-17 subset is characterized by an ability to produce the neutrophil-mobilizing cytokine IL-17 in response to stimulation with the cytokine IL-23, an IL-12-related cytokine released from antigen-presenting cells. There is now a growing body of evidence from animal models that the Th-17 subset plays an important role in host defence in the lungs and other organs. Altered IL-17 levels have also been demonstrated in human patients with asthma, exacerbations of cystic fibrosis or following lung transplantation. There is now also evidence that the Th-17 subset is functionally distinct from the Th-2 subset but little is known of the functional inter-relationship between the Th-1 and Th-17 cell subsets; this is particularly true in human lungs. It has been proposed that the Th-17 subset plays a unique role by linking the arms of innate and adaptive immunity. Thus, an improved understanding of the human correlate to the Th-17 subset may reveal new targets for pharmacotherapy against lung disorders that are characterized by aberrant innate responses in host defense.