Do we need new autoantibodies in lupus?

Systemic lupus erythematosus (SLE) is a complex disease, including serological differences between patients from different ethnicities [1]. Clinically, the range of illness is great - patients may have life-threatening manifestations, or the disease may not be much more than a nuisance. An SLE patient of ours once noted she was sitting next to someone else with SLE in the waiting area, but that they seemed to have nothing in common but the diagnosis. The patient was, understandably, suspicious that two people could share the diagnosis but otherwise not have any shared feature. That one must meet only 4 of 11 criteria to be classified as SLE demonstrates that this is indeed the case [2].Historically, and perhaps still, the major evidence that SLE is autoimmune is the presence of antibodies in the serum of SLE patients that bind self-structures. Here, too, the disease is extremely complex. Antinuclear antibody is a near-universal finding. Antibodies binding double-stranded DNA (dsDNA) are not nearly as common but are specific for the disease, and are strongly associated with kidney disease [3]. Antibodies to extractable nuclear antigens (anti-ENA) include anti-nRNP, anti-Sm, anti-Ro (or SSA) and anti-La (or SSB). Numerous other antibodies are found in the sera of patients with SLE, almost too numerous to keep up with.What, then, might be useful properties of autoantibodies in SLE? First, we should not forget that these antibodies have been useful in biology unrelated to clinical SLE. Anti-nRNP and anti-Sm played a critical part in defining the cellular role of the spliceosome [4]. In fact, without these naturally occurring antibodies to the spliceosome ribonucleoprotein components, we might still be working on how mature mRNA is produced.How are autoantibodies of use in regards to SLE itself [5]? One area is diagnosis. Clearly this is the case for some specificities. If a patient is not antinuclear antibody positive, then she (occasionally he) has almost no chance of