Rheumatology 1999; 38: 691-693
© 1999 British Society for Rheumatology
Editorials |
Antinuclear antibodies and lupus: causes and consequences
MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK
Systemic lupus erythematosus (SLE) is a disease of multiples. This extends from the clinical subsets and the likely genetic predisposition to the animal models that appear to have striking similarity to components of the human disease. Similarly, every year, the number of autoantibodies associated with lupus increases, although their provenance and role in disease pathogenesis remain unclear. Theoretically, autoantibodies could be `blamed' for many of the manifestations of disease; a recent report suggests that antibodies directed against erythropoietin might be responsible for the anaemia observed in some patients [1]. It is, however, antinuclear antibodies that have received most attention and research has focused on whether (and how) they directly cause disease (in particular nephritis), and their origins. Significant advances have been made in these areas in recent years.
It was ~40 yr ago that the association between anti-DNA antibodies and lupus was first described. Subsequently, it has become
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