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- W4313366154 abstract "Abstract Atopic dermatitis (AD) is a common Th2-biased chronic inflammatory skin disease. Major clinical manifestations include erythema, severe itchiness, and dry skin that impose a burden on patients and impairs their quality of life. Extensive research has been conducted to identify possible underlying mechanisms and develop therapeutic approaches. γδT cells, an understudied T cell population, play important roles in maintaining skin integrity in both human and mice. They are among the first responders to epithelial wounding and are a source of keratinocyte/fibroblast growth factors that promote wound repair. Hence, we wanted to investigate their behavior during wounding in an AD-like environment. Using a mouse model, we observed that γδT cell numbers are drastically decreased in atopic skin. Multiple factors contribute to this decrease, including insufficient activation, less proliferative capacity and increased cell death. These changes in γδT cell function are IL-4 dependent. Administration of IL-4 to wild type (WT) mice resulted in significant loss of γδT cells, and Il4−/− mice in the AD model showed numbers of γδT cells similar to WT controls. We further observed that the levels of keratinocyte/fibroblast growth factors are lower in AD animals, suggesting that loss of γδT cells could compromise re-epithelialization and repair following wounding. Collectively, our data indicate that in an atopic environment, γδT cells decrease drastically in an IL-4 dependent fashion, which may contribute to the aberrant wound healing process in AD animals." @default.
- W4313366154 created "2023-01-06" @default.
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- W4313366154 date "2019-05-01" @default.
- W4313366154 modified "2023-10-16" @default.
- W4313366154 title "The Th2 cytokine IL-4 mediates loss of skin γδT cells in atopic dermatitis" @default.
- W4313366154 doi "https://doi.org/10.4049/jimmunol.202.supp.182.41" @default.
- W4313366154 hasPublicationYear "2019" @default.
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