Researchers from the Institute for Molecular Bioscience (IMB) have made advances in understanding the cellular processes that occur during wound healing, skin cancer, and inflammatory skin conditions such as psoriasis.
They have pieced together the relationships between a number of proteins involved in the skin’s inflammatory response to infection or damage that occurs during ultraviolet (UV) radiation or wounding.
Dr Divya Ramnath from the IMB Centre for Inflammation and Disease Research said human skin provides an essential barrier against infection.
“Skin cells, called keratinocytes, raise the alarm when they detect infection or skin damage and start a chain reaction to restore a strong and healthy barrier,” she said.
“Previous research had shown that an important part of this process involves a protein called Toll-like receptor 3 (TLR3), which responds to molecules produced by invading microbes and cells damaged by UV or wounding.
“Another molecule that is also thought to be important in this process is a protein called interferon regulatory factor 6 (IRF6).
“We have now shown that TLR3 and IRF6 actually work together, and that they tell keratinocytes to secrete two signalling proteins called IL-23p19 and EBI3, which may help these cells and immune cells repair the skin.”
Associate Professor Matt Sweet from the IMB Centre for Inflammation and Disease Research said understanding how the components of this pathway fit together is an important step for treating skin diseases.
“This research is in its early stages, but it gives us a better understanding of how the body should respond to infection and skin damage,” he said.
“In the longer term, we may be able to use this knowledge to find out what’s going wrong in skin cancer, inflammatory skin conditions, or wounds that are slow to heal.
“We can then look for ways to correct these problems and work toward new treatments for those with such conditions.
“The aim of the IMB Centre for Inflammation and Disease Research is to identify the pathways that control inflammation and understand the progression from protective to pathological inflammation.
“Ultimately, this can help us to develop new therapies and drugs to treat and prevent the underlying causes of many inflammation-related diseases.”
The research was funded by the National Health and Medial Research Council, and was published in the journal Immunology and Cell Biology.
Contact: IMB Communications, communications@uq.edu.au, 07 3346 2134.
