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A glance at the medical journals at any time in the past 20 years will show that lupus, because of its widespread features, has been the focus of very intensive research. Indeed it has provided clues not only to the cause and mechanism of arthritis in general, but also some insight into a variety of other conditions. There is now an international journal, 'Lupus' which publishes monthly research papers on lupus from units all over the world.
Some of the most intensive research has looked into the suggestion that lupus is a viral disease. Clinically, there are many "flu-like" features, and a number of observations suggest that a virus may be the cause. One virus which has often come under suspicion (but not proven) is the 'E-B' virus of glandular fever. Some years ago, considerable interest was aroused by the finding of a viral "C-type" particle in biopsy tissue from patients with lupus. To date, this is the nearest direct evidence for a viral cause for SLE.
A number of small laboratory animals, notably a breed of mice glorying under the name of the "New Zealand Black/White" develop features of SLE. As well as many of the clinical features, their blood also contains LE cells and various antibodies including anti-DNA antibodies. Experimental work on the blood cells of these animals has thrown considerable light on SLE. It has shown how factors such as sex hormones, U V light, drugs etc affect the disease process, and doubtless will contribute to provide important information.
If it is difficult to explain what lupus is, then trying to explain or understand the immune defect in SLE compounds the difficulty. So much detailed work has been done on the immune system in SLE that lupus has become almost the standard by which other studies are made.
Put in scientific jargon, in active lupus there appears to be impairment of the suppressor cells. Perhaps the best analogy is the balance in a country between the police, or the forces of law and order (the suppressor "T" cells) and the population at large (B cells), some of which, if not properly governed, turn anarchic. There is normally a balance. In active lupus, the suppressor T cells seem to fail in their duty, and some B cells become out of control producing the various antibodies characteristic of the disease. Why the failure of the suppressor cells? We don't know, though, it is known that certain virus infections can affect these cells.
Clinicians have long recognised that there is a genetic element to lupus. Not only is there evidence from twin studies, but there are many examples of families with more than one lupus member.
The link almost certainly relates to an inherited abnormality in the patients’ immune system – as evidenced by the fact that other so-called ‘auto-immune’ diseases such as thyroid disease, Hughes Syndrome and Sjogren’s Syndrome are seen more frequently in the relatives of lupus patients.
Although the actual link or links have not been pinpointed, a huge research effort, using modern computer-based ‘finger printing’ techniques, is now in progress in an attempt to ‘map’ the genetic link more precisely.