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Ju Qiu

Researcher at Chinese Academy of Sciences

Publications -  41
Citations -  3044

Ju Qiu is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Innate lymphoid cell & Medicine. The author has an hindex of 16, co-authored 24 publications receiving 2378 citations. Previous affiliations of Ju Qiu include Albert Einstein College of Medicine & Northwestern University.

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The aryl hydrocarbon receptor regulates gut immunity through modulation of innate lymphoid cells.

TL;DR: It is shown that the aryl hydrocarbon receptor (Ahr) plays an essential role in RORγt(+) ILC maintenance and function, and a previously unrecognized physiological role for Ahr in promoting innate gut immunity by regulating R ORγt (+) I LCs is uncovered.
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Commensal bacteria protect against food allergen sensitization

TL;DR: It is shown here that sensitization to a food allergen is increased in mice that have been treated with antibiotics or are devoid of a commensal microbiota, and this data support the development of novel adjunctive probiotic therapies to potentiate the induction of tolerance to dietary allergens.
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Group 3 Innate Lymphoid Cells Inhibit T-Cell-Mediated Intestinal Inflammation through Aryl Hydrocarbon Receptor Signaling and Regulation of Microflora

TL;DR: An intricate balance between group 3 innate lymphoid cells and Th17 cells regulated by Ahr and commensal flora is revealed, raising the possibility that group 3 ILCs could negatively regulate Th 17 cells.
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Induction of innate lymphoid cell-derived interleukin-22 by the transcription factor STAT3 mediates protection against intestinal infection

TL;DR: Cancer therapies that utilize STAT3 inhibitors increase the risk for pathogen-mediated diarrhea through direct suppression of IL-22 from gut ILCs through directly binding to the Il22 locus.
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Growth Factor FGF2 Cooperates with Interleukin-17 to Repair Intestinal Epithelial Damage

TL;DR: Growth factor FGF2 synergized with interleukin-17 (IL-17) to induce genes for repairing of damaged epithelium through Act1-mediated direct signaling cross-talk in a DSS-induced colitis model.