| Literature DB >> 27034374 |
Pamela Y Chan1, Eugenio A Carrera Silva2, Dimitri De Kouchkovsky1, Leonel D Joannas1, Liming Hao3, Donglei Hu4, Scott Huntsman4, Celeste Eng4, Paula Licona-Limón1, Jason S Weinstein1, De'Broski R Herbert5, Joseph E Craft6, Richard A Flavell7, Silvia Repetto8, Jorge Correale9, Esteban G Burchard10, Dara G Torgerson4, Sourav Ghosh11, Carla V Rothlin12.
Abstract
Host responses against metazoan parasites or an array of environmental substances elicit type 2 immunity. Despite its protective function, type 2 immunity also drives allergic diseases. The mechanisms that regulate the magnitude of the type 2 response remain largely unknown. Here, we show that genetic ablation of a receptor tyrosine kinase encoded byTyro3in mice or the functional neutralization of its ortholog in human dendritic cells resulted in enhanced type 2 immunity. Furthermore, the TYRO3 agonist PROS1 was induced in T cells by the quintessential type 2 cytokine, interleukin-4. T cell-specificPros1knockouts phenocopied the loss ofTyro3 Thus, a PROS1-mediated feedback from adaptive immunity engages a rheostat, TYRO3, on innate immune cells to limit the intensity of type 2 responses.Entities:
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Year: 2016 PMID： 27034374 PMCID： PMC4935984 DOI： 10.1126/science.aaf1358
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728