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.
Copyright © 2016, American Association for the Advancement of Science.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptive Immunity / genetics*
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Animals
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Asthma / genetics
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Asthma / immunology*
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Blood Proteins / antagonists & inhibitors
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Blood Proteins / genetics
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Blood Proteins / metabolism
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Dendritic Cells / immunology
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Disease Models, Animal
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Gene Knockout Techniques
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Host-Parasite Interactions / genetics
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Host-Parasite Interactions / immunology*
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Humans
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Immunity, Innate / genetics*
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Interleukin-4 / immunology
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Interleukin-4 / pharmacology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Nippostrongylus / immunology
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Protein S
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Pyroglyphidae / immunology
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Receptor Protein-Tyrosine Kinases / genetics
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Receptor Protein-Tyrosine Kinases / physiology*
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Strongylida Infections / immunology
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T-Lymphocytes / immunology
Substances
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Blood Proteins
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PROS1 protein, human
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Protein S
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Interleukin-4
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Receptor Protein-Tyrosine Kinases
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TYRO3 protein, human
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Tyro3 protein, mouse