Scientists ID ‘first responders’ in wound healing

Researchers have identified a specific type of T cell that summons other immune cells to the site of skin injuries, shedding light on how these “first responders” contribute to wound healing.

Investigators with Scripps Research Institute sought to determine whether dendritic epidermal T cells (DETCs) - which are the only resident T cell population in the epidermis of mice - would produce interleukin-17A in response to a skin injury, according to a news release. IL-17A is considered a recruiter of other immune cells, promoting inflammation in most parts of the body.

In the mouse subjects that lacked IL-17A activity, wounds on their skin healed more slowly than normal, much like the subjects that lacked DETCs, researchers noted. When the scientists applied IL-17A to the skin of these subjects, the wounds were repaired. The rise in local IL-17A levels after skin injury depended on the activation of skin-resident DETCs, researchers found.

Adding normal DETCs from other subjects in the mice lacking IL-17A fully restored their wound-healing capacity.

“Only a subset produces IL-17A upon skin injury, although the surface markers on these cells seem identical to those of other DETCs,” Amanda S. MacLeod, M.D., senior researcher associate and lead author of the study, said in the news release. “Why only some DETCs respond to wounds in this way is something we plan to explore further.”

In another series of tests, researchers found that DETCs began producing IL-17A as soon as they detected damage signals from nearby keratinocytes. The surge in IL-17A levels induced the keratinocytes to make special proteins known to combat bacteria, viruses and other microbes.

“The ‘cross-talk’ between skin-resident T cells and nearby keratinocytes is critical for re-establishing the skin barrier following wounding,” Dr. MacLeod said.

The study findings were published online Sept. 24 in the Journal of Clinical Investigation.

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