Reactivity against complementary proteinase-3 is not increased in patients with PR3-ANCA-associated vasculitis.
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 autoanti...
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doaj-53bfbc2ede014ebf80519851df8c83d32020-11-24T22:04:59ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0163e1797210.1371/journal.pone.0017972Reactivity against complementary proteinase-3 is not increased in patients with PR3-ANCA-associated vasculitis.Henko TademaCees G M KallenbergCoen A StegemanPeter HeeringaThe 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.http://europepmc.org/articles/PMC3060099?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Henko Tadema Cees G M Kallenberg Coen A Stegeman Peter Heeringa |
spellingShingle |
Henko Tadema Cees G M Kallenberg Coen A Stegeman Peter Heeringa Reactivity against complementary proteinase-3 is not increased in patients with PR3-ANCA-associated vasculitis. PLoS ONE |
author_facet |
Henko Tadema Cees G M Kallenberg Coen A Stegeman Peter Heeringa |
author_sort |
Henko Tadema |
title |
Reactivity against complementary proteinase-3 is not increased in patients with PR3-ANCA-associated vasculitis. |
title_short |
Reactivity against complementary proteinase-3 is not increased in patients with PR3-ANCA-associated vasculitis. |
title_full |
Reactivity against complementary proteinase-3 is not increased in patients with PR3-ANCA-associated vasculitis. |
title_fullStr |
Reactivity against complementary proteinase-3 is not increased in patients with PR3-ANCA-associated vasculitis. |
title_full_unstemmed |
Reactivity against complementary proteinase-3 is not increased in patients with PR3-ANCA-associated vasculitis. |
title_sort |
reactivity against complementary proteinase-3 is not increased in patients with pr3-anca-associated vasculitis. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2011-01-01 |
description |
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. |
url |
http://europepmc.org/articles/PMC3060099?pdf=render |
work_keys_str_mv |
AT henkotadema reactivityagainstcomplementaryproteinase3isnotincreasedinpatientswithpr3ancaassociatedvasculitis AT ceesgmkallenberg reactivityagainstcomplementaryproteinase3isnotincreasedinpatientswithpr3ancaassociatedvasculitis AT coenastegeman reactivityagainstcomplementaryproteinase3isnotincreasedinpatientswithpr3ancaassociatedvasculitis AT peterheeringa reactivityagainstcomplementaryproteinase3isnotincreasedinpatientswithpr3ancaassociatedvasculitis |
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