Journal
IMMUNITY
Volume 50, Issue 4, Pages 975-991Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2019.03.018
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Asthma is a chronic inflammatory airway disease associated with type 2 cytokincs interleukin-4 (IL-4), IL. and IL-13, whicn promote airway eosinophilia, mucus overproduction, bronchial hyperresponsiveness (BHR), and immunogloubulin E (IgE) synthesis. However, only half of asthma patients exhibit signs of an exacerbated Type 2 response. Type 2-low asthma has different immune features: airway neutrophilia, obesity-related systemic inflammation, or in some cases, few signs of immune activation. Here, we review the cytokine networks driving asthma, placing these in cellular context and incorporating insights from cytokine-targeting therapies in the clinic. We discuss established and emerging paradigms in the context of the growing appreciation of disease heterogeneity and argue that the development of new and improved therapeutics require understanding the diverse mechanisms underlying the spectrum of asthma pathologies.
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