Reactivity against Complementary Proteinase-3 Is Not Increased in Patients with PR3-ANCA-Associated VasculitisTadema, H., Kallenberg, C. G. M., Stegeman, C. A. & Heeringa, P., 17-Mar-2011, In : PLoS ONE. 6, 3, 5 p., 17972.
Research output: Contribution to journal › Article › Academic › peer-review
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.
|Number of pages||5|
|Publication status||Published - 17-Mar-2011|
- ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES, ANTIRIBOSOMAL P AUTOANTIBODIES, STAPHYLOCOCCUS-AUREUS, SYSTEMIC VASCULITIS, MOLECULAR MIMICRY, NASAL CARRIAGE, AUTOIMMUNITY, INFECTIONS, ANTIBODIES, GRANULOMATOSIS