New data unexpectedly suggest that sera from patients with PR3-ANCA-associated vasculitis are less reactive than those of healthy controls to the 'antisense' product of the PR3 gene. How does this result fit with the theory of autoantigen complementarity, and the proposed role of anti-idiotypic antibodies in the development of ANCA-associated vasculitis?
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The authors' research activities are supported by Grant 2PO1DK from the National Institute of Diabetes and Digestive and Kidney Diseases/NIH.
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Preston, G., Falk, R. Does autoantigen complementarity underlie PR3-ANCA AAV?. Nat Rev Rheumatol 7, 439–440 (2011). https://doi.org/10.1038/nrrheum.2011.86
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DOI: https://doi.org/10.1038/nrrheum.2011.86
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