They found that these skin-resident immune cells function as "first responders" to skin injuries in part by producing the molecule known as interleukin-17A (IL-17A), which wards off infection and promotes wound healing.
"This appears to be a critical and unique component of mammals' defense against skin wounds, and we hope that it will point the way towards better therapies for people with difficulties in healing wounds," TSRI Professor and senior author of the study, Wendy L. Havran said.
Havran and other researchers have shown in recent years that special immune cells known as dendritic epidermal T cells (DETCs) are the only resident T cell population in the outer layer of skin (epidermis) of mice-and are resident in human skin, too.
These cells are now thought to serve as the immune system's principal sentinels in the skin-when they detect damage signals from nearby wounded skin cells, they summon other, non-skin-resident immune cells to the site of the wound.
Skin injuries in mice that have been bred to lack DETCs take much longer than normal to heal.
In the new study, Havran's laboratory looked for new ways in which DETCs contribute to wound healing.
The scientists found that DETCs are indeed the primary producers of IL-17A after skin injuries, but she observed that some and not all DETCs perform this function.
The study is published online by the Journal of Clinical Investigation.