Background: The chronic airway disease asthma causes significant burden to patients as well as the healthcare system with limited options for prevention or cure. Inadequate treatment strategies are most likely due to the complex heterogeneous nature of asthma. Furthermore, the severe asthma phenotype is characterized by the lack of a response to standard medication, namely, corticosteroids.
Scope of review: In the last several years it has been shown that the eosinophilic/atopic phenotype of asthma driven by T(H)2 mechanisms is not the only immunologic pathway contributing to disease. In fact, there has been evidence revealing that severe asthmatics in particular have neutrophilic inflammation, and this is associated with corticosteroid resistance. T(H)17 cells, a recently discovered lineage of T helper cells, play an important role in lung host defense against multiple pathogens via production of the cytokine IL-17. IL-17 promotes neutrophil production and chemotaxis via multiple factors.
Major conclusions: Mouse and human studies provide robust evidence that T(H)17 cells and IL-17 play a role in severe asthma and may contribute to corticosteroid resistance.
General significance: As we learn more about T(H)17 cells in severe asthma, the goal is to potentially target this pathway for treatment in the hope of significantly improving the quality of life for those children and adults affected with this disease. This article is part of a Special Issue entitled: Biochemistry of Asthma.
2011 Elsevier B.V. All rights reserved.