What controls ‘innate immunity’, our broad defence system that triggers inflammation when invading microbes, cellular damage or noxious stimuli are detected in the body?
That’s what Professor Matt Sweet’s laboratory is studying, seeking to understand how ‘pattern recognition receptors’ (PRRs) – the families of molecules that our immune system use to detect danger – work, in the hope of controlling them to treat inflammation-mediated diseases or harnessing their power to treat infectious diseases.
“Inflammation is tasked with trying to eliminate the danger, whether it’s an infection or an injury, and return the system to normal,” he says.
“We used to think inflammation had a role in only a limited number of conditions, but we now appreciate that it actually is driving disease, causing pain, discomfort and loss of function in many, many different diseases.”
Inflammation is the body’s way of focusing defences in an area where danger is afoot and where repair work is needed. But in chronic conditions – like arthritis, diabetes, Alzheimer’s, inflammatory bowel disease and chronic liver disease – inflammation often drives the loss of function of the particular organ, or organs, that is characteristic of the progression of that disease, for example joints in arthritis.
“We’re trying to understand how different pattern recognition receptors are awakened, how they drive antimicrobial responses that enable immune cells to kill infectious agents, and how they drive destructive inflammation in different disease settings,” he adds. “If we can understand how various pattern recognition receptors function, we can then manipulate them in different ways to combat both infectious and inflammatory diseases.”
Learn more about Matt's research at the Centre for Inflammation and Disease Research