Inflammation is a host response to tissue damage that leads to the production of cytokines that activate stromal cells including vascular endothelial cells. Activation of the latter enables the recruitment of white blood cells from the circulating blood to the damaged tissue. White blood cells help to clear the area of damaged tissue and microorganisms and start tissue repair. There is great interest in understanding these mechanisms because they can form the basis for development of new drugs useful to treat disorders of chronic inflammation such as rheumatoid arthritis, inflammatory disease, psoriasis and others. The aim of our research is to explore how the cytokine IL-33 and the Notch signalling system can be targeted to modulate inflammation and fibrosis.
Lack of interleukin-33 and its receptor does not prevent calcipotriol-induced atopic dermatitis-like inflammation in mice
Sci Rep, 10 (1), 6451
Interleukin-33 Signaling Controls the Development of Iron-Recycling Macrophages
Immunity, 52 (5), 782-793.e5
3PO inhibits inflammatory NFκB and stress-activated kinase signaling in primary human endothelial cells independently of its target PFKFB3
PLoS One, 15 (3), e0229395