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- W4366088093 abstract "IL-31 receptor blockade suppresses pruritus of atopic dermatitis. However, cell type-specific contributions of IL-31 receptor to itch, its expression mechanism, and the downstream signaling pathway to induce itch remain unknown. Here, using conditional knockout mice, we demonstrated that IL-31-induced itch required sensory neuronal IL-31 receptor and STAT3. IL-31 receptor was decreased in sensory neuronal STAT3 deficient mice, indicating that IL-31 receptor expression was dependent on STAT3 in sensory neurons. In addition, an acute treatment with the STAT3 inhibitor to wild type mice ameliorated IL-31-induced itch without reducing IL-31 receptor expression, which suggested that STAT3 activation was important for the itch-inducing signaling downstream of the IL-31 receptor. A cutaneous IL-31 injection induced the nuclear accumulation of activated STAT3 first in sensory neurons that abundantly expressed IL-31 receptor and then in other itch-transmitting neurons. Consistently, we found that IL-31 enhanced not only histamine-induced itch transmitted by IL-31 receptor-expressing neurons but also chloroquine-induced itch transmitted by other neuronal subsets. Finally, pruritus associated with dermatitis was partially dependent on sensory neuronal IL-31 receptor and strongly on sensory neuronal STAT3. Thus, sensory neuronal STAT3 is essential for IL-31-induced itch and further contributes to IL-31-independent inflammatory itch." @default.
- W4366088093 created "2023-04-19" @default.
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- W4366088093 date "2023-05-01" @default.
- W4366088093 modified "2023-09-27" @default.
- W4366088093 title "355 Sensory neuronal STAT3 is critical for IL-31 receptor expression and inflammatory itch" @default.
- W4366088093 doi "https://doi.org/10.1016/j.jid.2023.03.360" @default.
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