Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 210, Issue 13, Pages 2951-2965Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20130071
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Funding
- Medical Research Council UK [117512792, MC_UP_A253_1028]
- Deutsche Forschungsgemeinschaft (DFG) [TU 316/1-1]
- DGF (Klinische Forschergruppe 228 TP1) [PA 754/7]
- MRC [MC_U117512792, MC_UP_A253_1028] Funding Source: UKRI
- Medical Research Council [MC_U117512792, MC_UP_A253_1028] Funding Source: researchfish
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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.
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