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As a consequence, the restoration of tissue integrity and lung function was strongly impaired in the absence of IL-9 signaling. ILC2s, in contrast to Th2 cells, expressed high levels of the IL-9R, and IL-9 signaling was crucial for the survival of activated ILC2s in vitro. Furthermore, ILC2s in the lungs of infected mice required the IL-9R to up-regulate the antiapoptotic protein BCL-3 in vivo. This highlights a unique role for IL-9 as an autocrine amplifier of ILC2 function, promoting tissue repair in the recovery phase after helminth-induced lung inflammation.<\/jats:p>","DOI":"10.1084\/jem.20130071","type":"journal-article","created":{"date-parts":[[2013,11,18]],"date-time":"2013-11-18T23:46:02Z","timestamp":1384818362000},"page":"2951-2965","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":378,"title":["IL-9\u2013mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation"],"prefix":"10.1084","volume":"210","author":[{"given":"Jan-Eric","family":"Turner","sequence":"first","affiliation":[{"name":"Division of Molecular Immunology, Medical Research Council National Institute for Medical Research, London NW7 1AA, England, UK 1"},{"name":"III. 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