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New Kids on the BlockInnate Lymphoid Cells and Lung Inflammation: Group 2 Innate Lymphoid Cells and Type 2 Inflammation in the Lung

Timotheus Y. F. Halim, PhD; Andrew N. J. McKenzie, PhD
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From the MRC Laboratory of Molecular Biology, Cambridge, England.

Correspondence to: Timotheus Y. F. Halim, PhD, MRC Laboratory of Molecular Biology, Francis Crick Ave, Cambridge, CB2 0QH, England; e-mail: thalim@mrc-lmb.cam.ac.uk


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;144(5):1681-1686. doi:10.1378/chest.13-0911
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Inflammatory diseases of the lung are a major cause of morbidity and mortality. Allergic lung inflammation often stems from the overproduction of type 2 cytokines. The resulting type 2 inflammation is frequently caused by an inappropriate immune response to relatively harmless allergens and often associates with asthma. Until recently, the primary contributors of type 2 cytokines were believed to be T helper (Th) 2 cells. This concept was challenged by the discovery of group 2 innate lymphoid cells (ILC2s) in the lung, which represent a major source of type 2 cytokines during the acute inflammatory phase. Recent advances in our understanding of the regulation and development of ILC2 have redrawn the roadmap of type 2 inflammation. Indeed, ILC2s appear to be critical for the induction of adaptive immunity and, thus, play a central role for immune regulation. As one of the first responders in the entire Th2 cascade, ILC2 might serve as the early tile in a Th2 domino effect. As such, ILC2s present an attractive target for future drug development.


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