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IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation.
|Title||IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Turner J-E, Morrison PJ, Wilhelm C, Wilson M, Ahlfors H, Renauld J-C, Panzer U, Helmby H, Stockinger B|
|Journal||The Journal of experimental medicine|
|Date Published||2013 Dec 16|
IL-9 fate reporter mice established type 2 innate lymphoid cells (ILC2s) as major producers of this cytokine in vivo. Here we focus on the role of IL-9 and ILC2s during the lung stage of infection with Nippostrongylus brasiliensis, which results in substantial tissue damage. IL-9 receptor (IL-9R)-deficient mice displayed reduced numbers of ILC2s in the lung after infection, resulting in impaired IL-5, IL-13, and amphiregulin levels, despite undiminished numbers of Th2 cells. 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.
|Alternate Journal||J. Exp. Med.|