When beauty is skin deep: regulation of the wound response by caspase-8, RIPK3, and the inflammasome
- Author(s)
- Vince, JE;
- Details
- Publication Year 2015-08,Volume 135,Issue #8,Page 1936-9
- Journal Title
- J Invest Dermatol
- Publication Type
- Journal Article
- Abstract
- Caspase-8 downregulation is observed in the epidermis of wounded skin, whereas permanent epidermal caspase-8 deletion causes chronic skin inflammation, suggesting that caspase-8 is a critical regulator of skin homeostasis and, possibly, the wound response. In this issue, Lee et al. document how epidermal caspase-8 deletion, or cutaneous wounding, results in increased NF-kappaB activation to drive keratinocyte caspase-1 expression and subsequent secretion of the pro-inflammatory cytokines, IL-1beta and IL-1alpha. Consequently, loss of NF-kappaB activity, caspase-1, or the IL-1 receptor delays wound healing. Previous studies have documented how chronic skin inflammation in caspase-8-deficient mice is rescued by RIPK3 co-deletion. Therefore, targeting caspase-1, IL-1, or RIPK3 itself may benefit treatment of chronic inflammatory skin diseases, or where an inappropriate inflammatory response proves detrimental to wound healing, such as in type 2 diabetes.
- Publisher
- NPG
- Research Division(s)
- Inflammation
- PubMed ID
- 26174535
- Publisher's Version
- https://doi.org/10.1038/jid.2015.185
- NHMRC Grants
- NHMRC/1051210, NHMRC/1052598,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2015-07-20 02:23:54
Last Modified: 2015-07-20 02:51:28