Send to

Choose Destination
Atherosclerosis. 2014 Jan;232(1):242-8. doi: 10.1016/j.atherosclerosis.2013.11.041. Epub 2013 Nov 23.

Plasma autoantibodies against apolipoprotein B-100 peptide 210 in subclinical atherosclerosis.

Author information

Atherosclerosis Research Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. Electronic address:
Atherosclerosis Research Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Department of Clinical Sciences, Skåne University Hospital, Lund University, Malmö, Sweden.
Dipartimento di Scienze Farmacologiche e Biomolecolari, Università di Milano, Centro Cardiologico Monzino, IRCCS, Milan, Italy.
Atherosclerosis Research Unit, Department of Medicine, Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
Division of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
Foundation for Research in Health, Exercise and Nutrition, Kuopio Research Institute of Exercise Medicine, Kuopio, Finland.
Department of Medicine, University Medical Center Groningen, The Netherlands.
Internal Medicine, Angiology and Arteriosclerosis Diseases, Department of Clinical and Experimental Medicine, University of Perugia, Perugia, Italy.
Assistance Publique - Hopitaux de Paris, Service Endocrinologie-Metabolisme, Groupe Hôpitalier Pitie-Salpetriere, Unités de Prévention Cardiovasculaire, Paris, France.
Centre for Cardiovascular Genetics, University College London, United Kingdom.



Experimental studies have suggested that autoimmunity is involved in atherosclerosis and provided evidence that both protective and pro-atherogenic immune responses exist. This concept has received support from small clinical studies implicating autoantibodies directed against apolipoprotein B-100 (apoB-100) in human atherosclerosis. We examined circulating autoantibodies directed against native and malondialdehyde (MDA)-modified epitope p210 of apoB-100 (IgG-p210nat and IgM-p210MDA) in relation to early atherosclerosis in a large, European longitudinal cohort study of healthy high-risk individuals.


IgG-p210nat and IgM-p210MDA were quantified in baseline plasma samples of 3430 participants in the IMPROVE study and related to composite and segment-specific measures of severity and rate of progression of carotid intima-media thickness (cIMT) determined at baseline and after 30 months. IgM-p210MDA autoantibody levels were independently related to several cIMT measures both in the common carotid artery and in the carotid bulb, including measures of cIMT progression, higher levels being associated with lower cIMT or slower cIMT progression. Consistent inverse relationships were also found between plasma levels of IgG-p210nat and baseline composite measures of cIMT. These associations disappeared when adjusting for established and emerging risk factors, and there were no associations with rate of cIMT progression besides in certain secondary stratified analyses.


The present study provides further evidence of involvement of autoantibodies against native and MDA-modified apoB-100 peptide 210 in cardiovascular disease in humans and demonstrates that these associations are present already at a subclinical stage of the disease.


Carotid ultrasound; Intima-media thickness; Malondialdehyde-modified apoB-100 peptide 210; Native apoB-100 peptide 210; Progression

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center