The immunology of asthma

Asthma is typically thought to be a consequence of overreactive type II responses. In this Focus Review, Lambrecht and Hammad discuss the latest thinking on the etiology of asthma and the importance of alternative mechanisms such as ILC2, T H 9 and T H 17 cells. Asthma is a common disease that affects 300 million people worldwide. Given the large number of eosinophils in the airways of people with mild asthma, and verified by data from murine models, asthma was long considered the hallmark T helper type 2 (T H 2) disease of the airways. It is now known that some asthmatic inflammation is neutrophilic, controlled by the T H 17 subset of helper T cells, and that some eosinophilic inflammation is controlled by type 2 innate lymphoid cells (ILC2 cells) acting together with basophils. Here we discuss results from in-depth molecular studies of mouse models in light of the results from the first clinical trials targeting key cytokines in humans and describe the extraordinary heterogeneity of asthma.