EAS 2012 MILAN
>> Congress website & general info
>> Plenary sessions
>> Workshop sessions
Early-bird registration fee applies until March 12. Register now and save.
>> Congress registration
Professor Hansson and
Professor Pasterkamp
will take part in the
EAS 2012 Plenary Session
26 May, 2012, 08:30-10:30
CELLULAR AND HUMORAL FACTORS IN THE ARTERIAL WALL DETERMINE THE COURSE OF ATHEROGENESIS AND VASCULAR FUNCTION
Chaired by
Professor Alain Tedgui, France and
Professor Lale Tokgozoglu, Turkey
OTHER SPEAKERS AT EAS 2012
>> MARK MAJESKY
>> ULF LANDMESSER

Focus on... EAS 2012

As we count down to this year's Congress, each week we highlight speakers who will participate in EAS 2012.
This week the speakers in the spotlight are:

Professor Göran Hansson

IMMUNITY IN ATHEROSCLEROSIS


Göran Hansson is Professor of Cardiovascular Research at the Karolinska Institute and Head of the Cardiovascular Research Laboratory in the Center for Molecular Medicine at Karolinska University Hospital in Stockholm, Sweden. He is a previous recipient of the Anitschkow Prize from the European Atherosclerosis Society, as well as other prestigious awards. The focus of his research is immune and inflammatory mechanisms in atherosclerosis.

Atherosclerosis is a chronic inflammatory disease, elicited by cholesterol accumulation in the artery wall. The atherosclerotic plaque contains macrophages, T cells and other cells of the immune response, as well as cholesterol derived from low-density lipoprotein (LDL). Much progress has been made in understanding the immune mechanisms involved in atherosclerosis. Studies using gene-targeted mouse models have suggested that both immune modulation and immunization may reduce the progression of atherosclerotic disease.

T cells, present at all stages of atherosclerosis, play key roles in both initiation and progression of atherosclerotic plaque. Targeting T cells is attractive because of the antigen-specific, clonal nature of these cells.

Recent research has focused on identifying peptide fragments of apolipoprotein B100 (apoB100) which act as antigenic epitopes in triggering T cell activation. Conversely, blocking the immunological response involved in T cell recognition of apoB100 inhibits T cell activation and the secretion of proinflammatory cytokines, and also reduces atherosclerosis. These findings suggest therapeutic possibilities for the development of agents that selectively target T cells specific for a certain epitope.

Key references

1. Hansson GK, Hermansson A. The immune system in atherosclerosis. Nat Immunol 2011;12:204-12.

2. Hermansson A, Johansson DK, Ketelhuth DF, Andersson J, Zhou X, Hansson GK. Immunotherapy with tolerogenic apolipoprotein B-100-loaded dendritic cells attenuates atherosclerosis in hypercholesterolemic mice. Circulation 2011;123:1083-91.

3. Klingenberg R, Lebens M, Hermansson A, Fredrikson GN, Strodthoff D, Rudling M, Ketelhuth DF, Gerdes N, Holmgren J, Nilsson J, Hansson GK. Intranasal immunization with an apolipoprotein B-100 fusion protein induces antigen-specific regulatory T cells and reduces atherosclerosis. Arterioscler Thromb Vasc Biol 2010;30:946-52.

Professor Gerard Pasterkamp

UNDERSTANDING THE VULNERABLE PLAQUE – BASIS FOR TREATMENT OPTIONS 

Gerard Pasterkamp is Professor of Experimental Cardiology, Division Heart and Lungs, University Medical Centre Utrecht (UMCU), The Netherlands. His research has focused on arterial remodelling in atherosclerotic disease. He is the initiator and project leader of Athero-Express BioBank Studies, a longitudinal atherosclerotic plaque biobank from more than 2,000 patients.

Identifying individuals at risk of plaque rupture and subsequent clinical events remains a clinical challenge, given the limitations of risk stratification based on traditional markers and histological characteristics of the vulnerable plaque.

The Athero-Express project aims to identify novel local plaque markers, specifically genetic and molecular markers, that will aid in identification of individuals at risk. The premise underlying this approach is that atherosclerosis is a systemic disease and therefore all plaques in the vascular system provide information about the stability of the atherosclerotic lesions irrespective of their location.

Proteomic studies show that local plaque proteins may have strong predictive value for future cardiovascular events in all vascular territories. Subsequent research will aim to improve risk prediction by combining multiple biomarkers to define a plaque protein signature. Novel imaging techniques using specific targeting of cell surface receptors may help in ultimately translating study findings to the primary prevention setting.

Systems biology approaches, incorporating clinical, genetic and molecular data from such large bio-bank studies, are likely to have therapeutic application, especially in the context of a personalised management approach.

Key references

1. Peeters W, Moll FL, Vink A, van der Spek PJ, de Kleijn DP, de Vries JP, Verheijen JH, Newby AC, Pasterkamp G. Collagenase matrix metalloproteinase-8 expressed in atherosclerotic carotid plaques is associated with systemic cardiovascular outcome. Eur Heart J 2011;32:2314-25.

2. Herder C, Peeters W, Illig T, et al. RANTES/CCL5 and risk for coronary events: results from the MONICA/KORA Augsburg case-cohort, Athero-Express and CARDIoGRAM studies. PLoS One 2011;6:e25734.

3. Ylä-Herttuala S, Bentzon JF, Daemen M et al. Stabilisation of atherosclerotic plaques. Position paper of the European Society of Cardiology (ESC) Working Group on atherosclerosis and vascular biology. Thromb Haemost 2011;106:1-19.