"For people with inflammatory conditions such as allergic asthma, a certain type of immune cells – known as Th2 cells – is responsible for making a number of factors or molecules that cause inflammation," Ronchese explained.
"This excess inflammation can cause tissue damage, for example the inflamed and irritated skin of atopic eczema patients, or the typical shortness of breath experienced by asthma sufferers."
How Th2 cells picked up the ability to make these factors and molecules that caused inflammation largely remained a mystery.
"What is not yet completely clear is how those Th2 cells that we find in the lung or the skin or the gut develop," Ronchese said.
"When we look at the early stages of the immune response, Th2 cells look different, and don't really produce any of these inflammatory molecules.
"Somehow, they change – but we don't yet understand what drives these changes."
However, the research had now identified one such factor – the molecule TSLP – and its role in the development of Th2 cells that go on to cause an allergic response.
"It started with an observation," she said.
"We found that in some conditions where there is a lot of TSLP, inflammatory Th2 cells develop very quickly during the immune response."
After further investigation, her team found that TSLP had been turning these cells on, right from the start.
"TSLP accelerates the development of inflammatory cells in tissues that can cause disease, something that was not known previously," she said.
"People thought that TSLP acts mainly at different stages of the immune response, and maybe only in the lung and the skin.
"We're saying no, it has a broader role than that and really drive these cells to become inflammatory."
While the research team has not yet explored potential treatment opportunities of preventing TSLP in developing Th2 cells, the work did offer supporting evidence of TSLP blockers in existing clinical trials.