Researchers at Australia's Monash University have made a breakthrough which could eventually lead to much better lupus drugs - which would attack lupus, not the entire immune system.
One in 1000 Australians is affected by lupus. That's a lot of people on drugs which are aimed to switch off the immune system. Immunosuppressant drugs mean people with lupus are more likely to catch infections, and have more trouble fighting infections once caught.
From the report (see reference below):
In healthy people, B cells attack diseases by producing antibodies that destroy invading pathogens. In lupus sufferers, B cells are misdirected to produce autoantibodies – cells that destroy the patient's own healthy tissue. Most commonly, lupus affects the skin and joints, but it can also strike the brain, kidneys and almost anywhere in the body.
In order to survive, B cells rely on a particular protein – called B cell Activating Factor of the TNF Family (BAFF), however too much BAFF causes lupus to develop. Each B cell carries three different kinds of receptor that detect BAFF in the blood stream. The receptors are known as BAFF-R, BCMA, and TACI. It is the TACI receptor that responds to excesses of BAFF, becoming overstimulated and triggering production of even stronger autoantibodies to attack healthy tissue.
Researchers found that if the TACI receptor is deleted, the B cells remain intact but lupus doesn't develop no matter how much BAFF is in the blood.
Dr (Will) Figgett (from Monash Immunology Department) said that while B cells are vital to a healthy immune system, the TACI receptor itself is not crucial - the cell can fight most diseases without it.
This breakthrough means researchers developing lupus drugs have a very specific target. If future medications could turn off that receptor, without turning off the rest of the immune system, then if not a cure, we could have a treatment with far fewer side effects.
Donate to lupus research at Monash here: http://www.med.monash.edu.au/immunology/fundraising/lupus.html