Key result
Recent progress in tests determining the humoral response to HSP60 questions the durability of molecular mimicry as a hypothesis for arthritis pathogenesis.
New findings with increased specificity in testing for anti-HSP60 antibodies question the durability of molecular mimicry as a hypothesis for arthritis pathogenesis.
No change to arthritis practice warranted; challenges molecular mimicry hypothesis and leaves open alternative mechanisms.
As a result of the high sequence similarity between HSP60 proteins, found in both prokaryotic and eukaryotic cells, it has been suggested, but never concluded, that anti-HSP60 antibodies could be of importance in the pathology of arthritis diseases explained by a concept named molecular mimicry. In a number of clinical studies antibodies to both human and bacterial HSP60 have been detected in serum from patients with different inflammatory diseases, but divergent results have been published. Recent progress, however, has increased the specificity in tests used to determine the humoral response to HSP60. In this review, these new findings are compared with old questioning the durability of molecular mimicry as a hypothesis for arthritis pathogenesis.
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Gelsing et al. (2013) conducted a review in Arthritis. Anti-HSP60 antibodies was evaluated. Recent progress in tests determining the humoral response to HSP60 questions the durability of molecular mimicry as a hypothesis for arthritis pathogenesis.
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