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Yan Zheng

Researcher at Genentech

Publications -  16
Citations -  5134

Yan Zheng is an academic researcher from Genentech. The author has contributed to research in topics: Interleukin 22 & Medicine. The author has an hindex of 9, co-authored 11 publications receiving 4727 citations. Previous affiliations of Yan Zheng include Novo Nordisk & National Institutes of Health.

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Interleukin-22, a T H 17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis

TL;DR: The results suggest that TH17 cells, through the production of both IL-22 and IL-17, might have essential functions in host defence and in the pathogenesis of autoimmune diseases such as psoriasis.
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Interleukin-22 mediates early host defense against attaching and effacing bacterial pathogens

TL;DR: This work shows that interleukin-22 (IL-22) has a crucial role in the early phase of host defense against C. rodentium and identifies a new innate immune function for IL-22 in regulating early defense mechanisms against A/E bacterial pathogens.
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STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing

TL;DR: The data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22–dependent mucosal wound healing and Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis, and pathways associated with wound healing in IECs.
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Transcription factor c-Maf mediates the TGF-β-dependent suppression of IL-22 production in T H 17 cells

TL;DR: It is found that c-Maf bound to the Il22 promoter and was both necessary and sufficient for the TGF-β-dependent suppression of IL-22 production in TH17 cells.
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IL-22 bridges the lymphotoxin pathway with the maintenance of colonic lymphoid structures during infection with Citrobacter rodentium.

TL;DR: IL-22 signaling was sufficient to restore the organization of CLPs and ILFs and host defense against infection with C. rodentium in mice lacking lymphotoxin signals, which suggests that IL-22 connects theymphotoxin pathway to mucosal epithelial defense mechanisms.