期刊
SCIENCE
卷 352, 期 6281, 页码 99-103出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaf1358
关键词
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资金
- American Asthma Foundation
- NIH [R01 AI089824, T32 AI007019, T32 GM007205, HL088133, HL078885, HL004464, HL104608, HL117004]
- National Institute on Minority Health and Health Disparities [MD006902]
- Kolltan Pharmaceuticals
- Yale University Gershon-Trudeau Fellowship
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 by Tyro3 in 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-specific Pros1 knockouts phenocopied the loss of Tyro3. Thus, a PROS1-mediated feedback from adaptive immunity engages a rheostat, TYRO3, on innate immune cells to limit the intensity of type 2 responses.
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