Following infection, pathogenic microorganisms such as viruses and bacteria are initially recognised by specific receptors on the surface of neutrophils and macrophages. This triggers an immediate 'innate' immune response involving the production of proteins called chemokines and cytokines. These attract other immune cells to the sites of infection (inflammation) and also initiate the adaptive immune response that culminates in the production of protective antibodies and killing of infected cells.
The major focus of my group is to study a key MAP kinase signalling pathway activated during innate immune responses that is regulated by the protein kinase TPL-2.
Our current experiments are investigating the mechanism of TPL-2 activation by pathogen infection, and how TPL-2 regulation of cytokine and chemokine production in innate immune cells regulates inflammatory responses. In a new area of research for the laboratory (done in collaboration with Anne Bowcock at Imperial College London), we are also researching how the adaptor protein CARD14 activates NF-kB to trigger inflammation in the skin. Mutations in the gene encoding CARD14 lead to a high risk of developing psoriasis and psoriatic arthritis.