Aetiopathogenesis
Autoantibodies to ox-LDL in Sjögren’s syndrome: are they atheroprotective?
I. Cinoku1, C.P. Mavragani2, C.C. Tellis3, A. Nezos4, A.D. Tselepis5, H.M. Moutsopoulos6
- Department of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens; and Atherothrombosis Research Centre/Laboratory of Biochemistry, Department of Chemistry, University of Ioannina, Greece.
- Department of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens; and Department of Physiology, School of Medicine, National and Kapodistrian University of Athens, Greece.
- Atherothrombosis Research Centre/Laboratory of Biochemistry, Department of Chemistry, University of Ioannina, Greece.
- Department of Physiology, School of Medicine, National and Kapodistrian University of Athens, Greece. anezos@med.uoa.gr
- Atherothrombosis Research Centre/Laboratory of Biochemistry, Department of Chemistry, University of Ioannina, Greece.
- Department of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens; and Chair Medicine/Immunology, Academy of Athens, Greece.
CER11480
2018 Vol.36, N°3 ,Suppl.112
PI 0061, PF 0067
Aetiopathogenesis
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PMID: 30156537 [PubMed]
Received: 25/06/2018
Accepted : 19/07/2018
In Press: 13/08/2018
Published: 13/08/2018
Abstract
OBJECTIVES:
The higher incidence of atherosclerosis and cardiovascular disease (CVD) in patients with systemic autoimmune diseases cannot be attributed exclusively to traditional risk factors for CVD. Antibodies to oxidised Low Density Lipoprotein (ox-LDL) seem to have a crucial role in atherogenesis.
METHODS:
Sera from 63 consecutive patients with primary Sjögren’s syndrome (pSS), 121 with systemic lupus erythematosus (SLE), 79 with rheumatoid arthritis (RA) and 26 apparently healthy individuals were evaluated for the presence of antibodies to ox-LDL by ELISA. The femoral and/or carotid intima media thickness (IMT) and plaque formation as well as traditional CVD risk factors and disease-related features were recorded for all study participants. RESUKTS: Anti-ox-LDL antibody levels were significantly reduced in SS and RA patients, but not in SLE patients, compared to their healthy counterparts. Subsequently, SS patients were divided into two groups according to antibody levels to ox-LDL, using as cut off the median of each group studied. SS patients with high titres of antibodies to ox-LDL displayed higher rates of autoantibodies to Ro/SSA and La/SSB antigens, purpura, low complement levels and increased SS activity index. On the other hand, the high anti-ox-LDL group was characterised by reduced rates of carotid and/or femoral plaque after adjusting for potential confounders (OR [95%CI]: 0.14 [0.03-0.72]). Such associations were not shown in all other groups included in the study.
CONCLUSIONS:
These findings suggest that antibodies to ox-LDL, possibly resulting from B cell hyperactivity, might exert a protective role in the development of atherosclerosis among primary SS patients.