Stanford University School of Medicine.
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Early events in lupus humoral autoimmunity suggest initiation through molecular mimicry. McClain M, Heinlen LD, Dennis GJ, Roebuck J, Harley JB, James JA. Nature Medicine 11, 85-89 (2004).
First published online in Nature Medicine last December, this paper by Judith James of the Oklahoma University Health Sciences Center et. al investigates the origins of autoimmunity in systemic lupus erthematosus (SLE) by attempting to identify the environmental agents that could potentially incite autoimmunity. Using peptide arrays, the authors identified the initial autoantigenic epitope for some lupus patients positive for antibodies to 60 kDa Ro. This initial epitope directly cross-reacts with a peptide from the latent viral protein Epstein-Barr virus nuclear antigen-1 (EBNA-1).
Immunizing animals with either the first epitope of 60 kDa Ro or the cross-reactive EBNA-1 epitope resulted in the animals progressively developing autoantibodies binding multiple epitopes of Ro and spliceosomal autoantigens, the authors write. Eventually, the animals acquire clinical symptoms of lupus such as leukopenia, thrombocytopenia and renal dysfunction. As a result, the authors conclude that some humoral autoimmunity in human lupus arises through molecular mimicry between EBNA-1 and lupus autoantigens, and they suspect that Epstein-Barr virus plays an etiologic role in SLE.