PMID- 21437233
OWN - NLM
STAT- MEDLINE
DCOM- 20110705
LR  - 20220223
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 6
IP  - 3
DP  - 2011 Mar 17
TI  - Reactivity against complementary proteinase-3 is not increased in patients with 
      PR3-ANCA-associated vasculitis.
PG  - e17972
LID - 10.1371/journal.pone.0017972 [doi]
LID - e17972
AB  - 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.
FAU - Tadema, Henko
AU  - Tadema H
AD  - Department of Rheumatology and Clinical Immunology, University Medical Center 
      Groningen, University of Groningen, Groningen, The Netherlands. 
      h.tadema@reuma.umcg.nl
FAU - Kallenberg, Cees G M
AU  - Kallenberg CG
FAU - Stegeman, Coen A
AU  - Stegeman CA
FAU - Heeringa, Peter
AU  - Heeringa P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110317
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antibodies, Antineutrophil Cytoplasmic)
RN  - EC 3.4.21.76 (Myeloblastin)
SB  - IM
MH  - Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/blood/*immunology
MH  - Antibodies, Antineutrophil Cytoplasmic/*immunology
MH  - Case-Control Studies
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myeloblastin/*immunology
PMC - PMC3060099
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2011/03/26 06:00
MHDA- 2011/07/06 06:00
PMCR- 2011/03/17
CRDT- 2011/03/26 06:00
PHST- 2011/01/11 00:00 [received]
PHST- 2011/02/16 00:00 [accepted]
PHST- 2011/03/26 06:00 [entrez]
PHST- 2011/03/26 06:00 [pubmed]
PHST- 2011/07/06 06:00 [medline]
PHST- 2011/03/17 00:00 [pmc-release]
AID - PONE-D-11-01711 [pii]
AID - 10.1371/journal.pone.0017972 [doi]
PST - epublish
SO  - PLoS One. 2011 Mar 17;6(3):e17972. doi: 10.1371/journal.pone.0017972.