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Decreased levels of autoantibodies against apolipoprotein B-100 antigens are associated with cardiovascular disease in systemic lupus erythematosus.

Svenugnsson, Elisabet ; Engelbertsen, Daniel LU ; Wigren, Maria LU ; Gustafsson, Johanna T ; Gunnarsson, Iva ; Elvin, Kerstin ; Jensen-Urstad, Kerstin ; Nordin Fredrikson, Gunilla LU and Nilsson, Jan LU (2015) In Clinical and Experimental Immunology 181(3). p.417-426
Abstract
Increased production of autoantibodies is a characteristic feature of systemic lupus erythematosus (SLE) and there is evidence that several of these autoantibodies may contribute to the increased cardiovascular disease (CVD) in SLE. Autoantibodies against the apolipoprotein (apo) B-100 peptides p45 and p210 have been associated with a lower CVD risk in non-SLE cohorts. The aim of the present study was to investigate how SLE affects the occurrence of these potentially protective autoantibodies. The study cohort consisted of 434 SLE patients and 322 age and sex-matched population controls. Antibodies against native and malondialdehyde (MDA)-modified p45 and p210 were measured by ELISA. SLE patients had significantly lower levels of p210 IgG... (More)
Increased production of autoantibodies is a characteristic feature of systemic lupus erythematosus (SLE) and there is evidence that several of these autoantibodies may contribute to the increased cardiovascular disease (CVD) in SLE. Autoantibodies against the apolipoprotein (apo) B-100 peptides p45 and p210 have been associated with a lower CVD risk in non-SLE cohorts. The aim of the present study was to investigate how SLE affects the occurrence of these potentially protective autoantibodies. The study cohort consisted of 434 SLE patients and 322 age and sex-matched population controls. Antibodies against native and malondialdehyde (MDA)-modified p45 and p210 were measured by ELISA. SLE patients had significantly lower levels of p210 IgG and p45 IgM (both the native and MDA-modified forms). SLE patients with manifest CVD (myocardial infarction, ischemic cerebrovascular disease or peripheral vascular disease) had lower levels p210 IgG and p45 IgM than SLE patients without CVD. Decreased levels of these autoantibodies were also observed in SLE patients with permanent organ damage as assessed by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (ACR) Damage Index (SDI). The present findings show that patients with SLE, a condition generally characterized by abundance of autoantibodies of multiple specificities, have reduced levels of antibodies against the apo B-100 antigens p45 and p210 and that the levels of these antibodies are further reduced in SLE patients with CVD. These observations suggest the possibility that an impaired antibody-mediated removal of damaged LDL particles may contribute to the development of vascular complications and organ damage in SLE. This article is protected by copyright. All rights reserved. (Less)
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author
; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Clinical and Experimental Immunology
volume
181
issue
3
pages
417 - 426
publisher
British Society for Immunology
external identifiers
  • pmid:25959453
  • wos:000359731700004
  • scopus:84939267562
  • pmid:25959453
ISSN
0009-9104
DOI
10.1111/cei.12651
language
English
LU publication?
yes
id
5c09d13e-6994-4e12-b5c4-9acb1920912f (old id 5453570)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25959453?dopt=Abstract
date added to LUP
2016-04-01 10:48:51
date last changed
2022-04-20 06:30:44
@article{5c09d13e-6994-4e12-b5c4-9acb1920912f,
  abstract     = {{Increased production of autoantibodies is a characteristic feature of systemic lupus erythematosus (SLE) and there is evidence that several of these autoantibodies may contribute to the increased cardiovascular disease (CVD) in SLE. Autoantibodies against the apolipoprotein (apo) B-100 peptides p45 and p210 have been associated with a lower CVD risk in non-SLE cohorts. The aim of the present study was to investigate how SLE affects the occurrence of these potentially protective autoantibodies. The study cohort consisted of 434 SLE patients and 322 age and sex-matched population controls. Antibodies against native and malondialdehyde (MDA)-modified p45 and p210 were measured by ELISA. SLE patients had significantly lower levels of p210 IgG and p45 IgM (both the native and MDA-modified forms). SLE patients with manifest CVD (myocardial infarction, ischemic cerebrovascular disease or peripheral vascular disease) had lower levels p210 IgG and p45 IgM than SLE patients without CVD. Decreased levels of these autoantibodies were also observed in SLE patients with permanent organ damage as assessed by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (ACR) Damage Index (SDI). The present findings show that patients with SLE, a condition generally characterized by abundance of autoantibodies of multiple specificities, have reduced levels of antibodies against the apo B-100 antigens p45 and p210 and that the levels of these antibodies are further reduced in SLE patients with CVD. These observations suggest the possibility that an impaired antibody-mediated removal of damaged LDL particles may contribute to the development of vascular complications and organ damage in SLE. This article is protected by copyright. All rights reserved.}},
  author       = {{Svenugnsson, Elisabet and Engelbertsen, Daniel and Wigren, Maria and Gustafsson, Johanna T and Gunnarsson, Iva and Elvin, Kerstin and Jensen-Urstad, Kerstin and Nordin Fredrikson, Gunilla and Nilsson, Jan}},
  issn         = {{0009-9104}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{417--426}},
  publisher    = {{British Society for Immunology}},
  series       = {{Clinical and Experimental Immunology}},
  title        = {{Decreased levels of autoantibodies against apolipoprotein B-100 antigens are associated with cardiovascular disease in systemic lupus erythematosus.}},
  url          = {{https://lup.lub.lu.se/search/files/2156214/8776948.pdf}},
  doi          = {{10.1111/cei.12651}},
  volume       = {{181}},
  year         = {{2015}},
}