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- W4313366178 abstract "Abstract Epidermal resident γδ T cells are key players in the wound healing response, providing growth factors and cytokines that promote keratinocyte proliferation following recognition of damaged self. These cells are known to be unresponsive in chronic wounds and as such represent a novel target for new wound healing therapies. In this study we seek to modulate the γδ T cell response in chronic wounds through the identification, characterization, and delivery of keratinocyte-expressed proteins that comprise a “wound signature” allowing γδ T cells to recognize and respond to epithelial damage. We have identified a set of target genes though RNA-seq analysis which are upregulated following wounding in mice and correspond to membrane-bound and secreted proteins available for interactions with neighboring cells. Candidate gene expression was measured following wounding of human skin tissue, and ICAM1, CRISPLD2, and HSPA8 were shown to also be significantly upregulated in human skin wound samples. Hspa8 and ICAM-1 have been validated through in vitro assays to activate γδ T cells, and these proteins have been chosen for in vivo delivery. In order to deliver these candidate proteins into in vivo wound models we have developed a hydrogel-based delivery system with a highly tunable time frame of release. This system improves the retention of protein cargo at the wounds site post-wounding in mice and is being used to administer our candidate proteins into mouse models of non-healing wounds to assess effects on acceleration of tissue repair." @default.
- W4313366178 created "2023-01-06" @default.
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- W4313366178 date "2019-05-01" @default.
- W4313366178 modified "2023-09-26" @default.
- W4313366178 title "γδ T cell activation in response to a keratinocyte wound signature" @default.
- W4313366178 doi "https://doi.org/10.4049/jimmunol.202.supp.60.12" @default.
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