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Author
dc.contributor.author
Prechl, József 
Author
dc.contributor.author
Papp, Krisztián 
Author
dc.contributor.author
Z, Herincs 
Author
dc.contributor.author
H, Peterfy 
Author
dc.contributor.author
Lóránd, Veronika 
Author
dc.contributor.author
Szittner, Zoltán 
Author
dc.contributor.author
Czirják, László 
Availability Date
dc.date.accessioned
2016-04-11T11:44:47Z
Availability Date
dc.date.available
2016-04-11T11:44:47Z
Release
dc.date.issued
2016
Issn
dc.identifier.issn
1932-6203
uri
dc.identifier.uri
http://hdl.handle.net/10831/30149
Abstract
dc.description.abstract
Systemic lupus erythematosus is a chronic autoimmune disease with multifactorial ethiopathogenesis. The complement system is involved in both the early and late stages of disease development and organ damage. To better understand autoantibody mediated complement consumption we examined ex vivo immune complex formation on autoantigen arrays. We recruited patients with SLE (n = 211), with other systemic autoimmune diseases (n = 65) and non-autoimmune control subjects (n = 149). Standard clinical and laboratory data were collected and serum complement levels were determined. The genotype of SNP rs1143679 in the ITGAM gene was also determined. Ex vivo formation of immune complexes, with respect to IgM, IgG, complement C4 and C3 binding, was examined using a functional immunoassay on autoantigen microarray comprising nucleic acids, proteins and lipids. Complement consumption of nucleic acids increased upon binding of IgM and IgG even when serum complement levels were decreased due to consumption in SLE patients. A negative correlation between serum complement levels and ex vivo complement deposition on nucleic acid autoantigens is demonstrated. On the contrary, complement deposition on tested protein and lipid autoantigens showed positive correlation with C4 levels. Genetic analysis revealed that the non-synonymous variant rs1143679 in complement receptor type 3 is associated with an increased production of anti-dsDNA IgG antibodies. Notwithstanding, homozygous carriers of the previously reported susceptible allele (AA) had lower levels of dsDNA specific IgM among SLE patients. Both the non-synonymous variant rs1143679 and the high ratio of nucleic acid specific IgG/IgM were associated with multiple organ involvement. In summary, secondary complement deficiency in SLE does not impair opsonization of nucleic-acid-containing autoantigens but does affect other antigens and potentially other complement dependent processes. Dysfunction of the receptor recognizing complement opsonized immune complexes promotes the development of class-switched autoantibodies targeting nucleic acids.
Language
dc.language
Angol
Rent
dc.publisher
Public Library of Science (PLoS)
Contact information
dc.relation.ispartof
urn:issn:1932-6203
Title
dc.title
Serological and Genetic Evidence for Altered Complement System Functionality in Systemic Lupus Erythematosus: Findings of the GAPAID Consortium.
Type
dc.type
folyóiratcikk
Date Change
dc.date.updated
2016-04-05T14:23:52Z
Language
dc.language.rfc3066
eng
Scope
dc.format.page
e0150685
Doi ID
dc.identifier.doi
doi:10.1371/journal.pone.0150685
MTMT ID
dc.identifier.mtmt
3036334
Issue Number
dc.identifier.issue
3
Journal
dc.identifier.jtitle
PLOS ONE
Volume Number
dc.identifier.volume
11
Release Date
dc.description.issuedate
2016
Author Details
dc.description.author
Prechl, József : 10015636 (ELTE/TTK/Bio_I/MTA-ELTE Immunológiai Kutatócsoport)
Author Details
dc.description.author
Papp, Krisztián : 10017315 (ELTE/TTK/Bio_I/MTA-ELTE Immunológiai Kutatócsoport)
Pubmed ID
dc.identifier.pubmed
26950932
Author institution
dc.contributor.department
ELTE/TTK/Bio_I/MTA-ELTE Immunológiai Kutatócsoport
Author institution
dc.contributor.department
ELTE/TTK/Bio_I/MTA-ELTE Immunológiai Kutatócsoport
Author MTMT ID
dc.contributor.mtmtid
10015636
Author MTMT ID
dc.contributor.mtmtid
10017315
Uploader's email
dc.description.submitteremail
jprechl@gmail.com
Uploader Name
dc.description.submittername
Prechl József
ID Uploader
dc.identifier.submitter
10015636


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Serological and Genetic Evidence for Altered Complement System Functionality in Systemic Lupus Erythematosus: Findings of the GAPAID Consortium.
 

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