In autoimmune diseases, the immune system attacks its own tissues, leading to inflammation. The membranes lining the joints are often affected and over time can suffer irreversible damage.
But the damage can go well beyond that, devastating the kidneys, lungs, skin, and eyes.
Why do our defences suddenly turn on us? One of the most frustrating things about inflammation in most chronic diseases is that we don’t know exactly what triggers it.
Viral or bacterial infection may play a major role, but environmental and hereditary factors are also at play.
We know, for example, that there is a strong genetic component in up to 60 per cent of cases of rheumatoid arthritis, an autoimmune disease associated with inflammation in the joints and other tissues. Ageing, on the other hand, is a major factor in systemic lupus erythematosus, although as it is most common in women and specific ethnicities, it also has a hereditary component.
The inflammation causing these diseases starts out as a normal response.
“The attack phase of inflammation is designed to be short and robust and is normally followed by a repair phase to heal any bystander damage done to surrounding tissues,” says IMB’s Professor Jennifer Stow.
But in chronic inflammatory and autoimmune diseases, the attack phase never ends.
The repair phase is also impaired or inadequate in these chronic conditions, resulting in tissue damage that causes pain and leads to loss of organ function.
With no single cure currently available for autoimmune diseases, researchers have turned to inflammation as the target for possible treatments. One strategy has been to look at how immune cells are activated in the first place, and the role of cytokines – chemical messengers that help to orchestrate the body’s responses.
One of the most powerful chemical messengers is tumour necrosis factor, or TNF, which can be released by immune cells to kill tumours. In inflammatory and autoimmune diseases, the excessive release of TNF promotes ongoing waves of inflammation, causing tissue damage, pain and suffering.
Researchers found that blocking the action of TNF with drugs like Infliximab and Enbrel helps many patients with rheumatoid arthritis.
The results have been impressive, with 70 per cent of rheumatoid arthritis patients showing reduced inflammation and symptoms.
“Unfortunately these treatments don’t do much for the other 30 per cent of patients,” says Professor Stow. “But they stand as a wonderful proof of concept that we can successfully target the messengers to turn off inflammation. The job of researchers now is to identify additional drug targets to treat all patients.”