Scientists have found a possible genetic cause for the potentially fatal condition lupus, which could lead to the development of a drug treatment.
Genetic experiments on mice found that a single defect in the messaging system between cells caused a severe auto-immune disease which resembles lupus.
The breakthrough could lead to new treatments not only for lupus, but also for a range of other auto-immune diseases.
These diseases result from a malfunction in the body's defence mechanism, whereby instead of attacking foreign invaders, the immune system starts to attack the tissues of the body.
In lupus patients the immune system targets the joints, muscles and organs.
This can lead to a range of symptoms including joint pain, fatigue, rashes on the head and upper body, and persistent flu-like symptoms.
In severe cases, the heart and lungs can become inflamed. There is also a risk of kidney failure and arthritis.
Thousands of sufferers
It is estimated 10,000 people in the UK are affected by systemic lupus erthyematosus (SLE).
It particularly affects young people and children. It is ten times more common in women and four times more likely to occur in Afro-Caribbean and Asian people than whites.
Professor of medicine Arthur Weiss from the University of California in San Francisco, who led the research team, said: "While researchers have studied the disease intensively, the cause - or causes - have proven difficult to pin down.
"It may well be that at least part of the answer to the puzzle lies with a very small change in a signalling problem that underlies many different cell functions."
The researchers say that only one parent would need to carry the defect to pass the condition on to their children.
Until now, the only possible genetic causes identified for auto-immune diseases have had to be carried by both parents before they show up in their children.
Scientists say the finding suggests the range of symptoms associated with lupus could all derive from a single defect.
They found a "lupus-like syndrome" resulted from a single change in a key protein found on the surface of immune-system cells.
The protein normally receives and triggers internal responses in cells.
The researchers say it could be the "chemical switch" that stops the body producing too many immune cells when it is fighting infections.
More experiments are now planned by the San Francisco research team, aimed at discovering if this "signalling problem" found in mice is replicated in humans.
If so, a drug which can repair the signalling process in patients with lupus or other auto-immune diseases could be developed.
The research is published in the journal Cell.