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.
Hypo-osmotic stress induces the epithelial alarmin IL-33 in the colonic barrier of ulcerative colitis
Sci Rep, 12 (1), 11550
Activated, Pro-Inflammatory Th1, Th17, and Memory CD4+ T Cells and B Cells Are Involved in Delayed-Type Hypersensitivity Arthritis (DTHA) Inflammation and Paw Swelling in Mice
Front Immunol, 12, 689057
A novel somatic mutation in GNB2 provides new insights to the pathogenesis of Sturge-Weber syndrome
Hum Mol Genet, 30 (21), 1919-1931