Recent research led by Elaine Fuchs at Rockefeller University has unveiled an IL24-driven mechanism that facilitates skin tissue repair by responding to injury signals instead of pathogens. This discovery introduces an evolutionary pathway that enhances tissue regeneration during hypoxic conditions, typically resulting from blood vessel disruption following an injury. The study, published in Cell, highlights how epidermal stem cells at the wound’s edge secrete IL24 in reaction to low oxygen levels, triggering a cascade of healing processes without the presence of infections.
IL24 acts as a signaling molecule, orchestrating the repair process by regulating various skin cells, including epithelial cells, fibroblasts, and endothelial cells, which express IL24 receptors. Researchers found that in germ-free mice, the IL24 signaling pathway activated during wounds remained intact, indicating its independence from microbial factors. Additionally, experiments on genetically modified mice lacking IL24 demonstrated significantly delayed healing, underscoring its crucial role in tissue repair.
The findings suggest that IL24 may also play a role in healing mechanisms across other epithelial tissues in the body, such as the lungs and colon. The study concludes that IL24 represents a vital component of injury response pathways, evolutionary linked to the response to pathogens.
