Scientists at Fujita Health University, Japan, have discovered how deficiencies of the IL-36Ra protein — caused by mutations in the IL36RN gene — delay wound healing via the flooding of the wound with several types of immune cells. However, by inhibiting the functioning of proteins and the signaling pathways involved in activating the immune system at a wound, this delay can be offset. These findings could aid efforts to develop ways of regulating wound healing in IL36RN mutation-related skin disorders.
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