Zurich – Researchers at the University of Zurich (UZH) are on the trail of an approach to accelerate wound healing. It is based on immune checkpoint inhibitors that regulate the immune response. Nicole Joller’s team has discovered how the inhibitor TIGIT promotes tissue repair.
(CONNECT) A team of UZH researchers led by Nicole Joller, Professor of Immunology at the University's Institute of Quantitative Biomedicine, is researching new possibilities for tissue healing. To this end, they have investigated the mode of action of the immune checkpoint inhibitor TIGIT, the UZH reports in a press release. Immune checkpoint inhibitors sit on the surface of immune cells and protect the body from an excessive immune response.
It is known from previous research that TIGIT protects mice to a certain extent against tissue damage in the event of infection. However, the exact mechanisms were previously unknown, Joller explains in the press release. Your team has now solved this mystery.
First, the researchers demonstrated the direct link between TIGIT and wound healing: In animal experiments, mice without the gene for TIGIT developed greater tissue damage after an infection than the control group with TIGIT. In the next step, immune cells with and without TIGIT on the surface were compared. Here, only immune cells with TIGIT reacted to the virus with a growth factor that activates repair mechanisms.
"This sheds new light on the balance between immune defense and tissue protection," says Joller. According to her, the research results help to better understand the tissue damage caused by viral infections. They could also contribute to the development of new therapies for liver fibrosis or the healing of chronic wounds, for example. "There is an opportunity here to activate the TIGIT checkpoint and thus accelerate regeneration," says Joller. ce/hs
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