Journal
MUCOSAL IMMUNOLOGY
Volume 9, Issue 1, Pages 275-286Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2015.59
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Funding
- National Institutes of Health [AI026918, AI030663, AI119944]
- Howard Hughes Medical Institute
- Sandler Asthma Basic Research Center at the University of California, San Francisco
- UCSF Medical Scientist Training Program
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL128903, P01HL107202] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI030663, K08AI113143, T32AI007334, R01AI026918, R37AI026918] Funding Source: NIH RePORTER
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Group 2 innate lymphoid cells (ILC2s) have an important role in acute allergic lung inflammation. Given their distribution and function, lung ILC2s are hypothesized to coordinate epithelial responses to the external environment; however, how barrier surveillance is linked to ILC2 activation remains unclear. Here, we demonstrate that alveolar type II cells are the main source of interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP) generated in response to chitin or migratory helminths. IL-33 and TSLP synergistically induce an interferon regulatory factor 4 (IRF4)-IL-9 program in ILC2s, and autocrine IL-9 promotes rapid IL-5 and IL-13 production required for optimal epithelial responses in the conducting airways. Thus, ILC2s link alveolar function to regulation of airway flow, revealing a key interaction between resident lymphoid and structural cells that might underlie similar organizational hierarchies in other organs.
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