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Reactivity against Complementary Proteinase-3 Is Not Increased in Patients with PR3-ANCA-Associated Vasculitis

Tadema, H., Kallenberg, C. G. M., Stegeman, C. A. & Heeringa, P., 17-Mar-2011, In : PLoS ONE. 6, 3, 5 p., 17972.

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The etiology of anti-neutrophil cytoplasmic antibodies (ANCA) associated vasculitides (AAV) is unknown, but the association between infections and autoimmunity has been studied extensively. In 2004, a novel theory was proposed that could link infection and autoimmunity. This 'theory of autoantigen complementarity' was based on the serendipitous finding of antibodies against complementary-PR3 (cPR3) in patients with PR3-ANCA-associated vasculitis. cPR3 demonstrated homology to several bacterial proteins, and it was hypothesized that PR3-ANCA develop in response to anti-cPR3 antibodies, as a consequence of the anti-idiotypic network. These data have not been confirmed in other patient cohorts. We investigated the presence of anti-cPR3 antibodies in a Dutch cohort of PR3-ANCA-associated vasculitis patients. Anti-cPR3 reactivity was determined in serum using ELISA. Two separate batches of cPR3 were used to determine reactivity in two separate cohorts of PR3-ANCA-associated vasculitis patients. We found that anti-cPR3-reactivity was not increased in our PR3-ANCA-associated vasculitis patients, in comparison to control groups. Further research will be necessary to prove the concept of autoantigen complementarity in autoimmune diseases.

Original languageEnglish
Article number17972
Number of pages5
JournalPLoS ONE
Volume6
Issue number3
Publication statusPublished - 17-Mar-2011

    Keywords

  • ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES, ANTIRIBOSOMAL P AUTOANTIBODIES, STAPHYLOCOCCUS-AUREUS, SYSTEMIC VASCULITIS, MOLECULAR MIMICRY, NASAL CARRIAGE, AUTOIMMUNITY, INFECTIONS, ANTIBODIES, GRANULOMATOSIS

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