A single gene that helps form the skin’s surface also keeps crucial immune cells alive, according to new research from Ben-Gurion University of the Negev published in Cell Reports.
Scientists found that the gene, known as ZNF750, does more than shape healthy skin. It also allows Langerhans cells, the body’s first responders to germs at the skin’s surface, to survive where they are needed most.
To test this, researchers engineered mice so the gene was removed only from skin cells, leaving the immune system untouched. The result surprised them. Immune cells deep in the skin remained normal, but Langerhans cells in the outer layer nearly vanished. The immune cells themselves were healthy; they simply could not stay alive without support from the surrounding skin.
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The team traced the problem to a substance called IL-34, which skin cells produce to help these immune cells survive. Without ZNF750, IL-34 levels fell sharply, cutting off the signal that keeps Langerhans cells in place.
“Skin cells don’t just form a barrier,” said Prof. Idan Cohen. “They create the conditions that allow immune cells to live and function.” Prof. Roi Gazit added that the findings show the skin plays an active role in maintaining the body’s immune defenses.
The discovery may help explain why certain skin diseases affect both the skin’s structure and its immune balance. Changes in ZNF750 are already linked to rare inherited skin disorders and to psoriasis. People with psoriasis and atopic dermatitis are also known to have fewer Langerhans cells.
Researchers say the work opens the door to new ways of thinking about treatment, including the possibility of restoring signals that help immune cells survive.
The study was conducted by Lotem Adar, Sony Sharma, Bar Schwartz, and colleagues in the laboratories of Cohen and Gazit at Ben-Gurion University of the Negev, with funding from the Israel Science Foundation.