Keynote: Göran K. Hansson

Göran K. Hansson

Stockholm, Sweden

The EAS is delighted to announce that one of the Keynote Lectures at the 2017 EAS Congress in Prague will be given by Professor Göran K. Hansson, Professor of Experimental Cardiovascular Research, Karolinska Institutet, Sweden.

Göran K. Hansson is Professor of Cardiovascular Research at Karolinska Institute and works in the Department of Medicine at Karolinska University Hospital and its Center for Molecular Medicine. He received his MD and PhD at Gothenburg University School of Medicine in Sweden, was a postdoctoral fellow at the University of Washington in Seattle, WA, USA, and has been Professor of Cell Biology at Gothenburg University and Leducq Visiting Professor at Harvard Medical School in Boston, MA, USA.

From 1 July 2015, Dr Hansson is the Secretary General of the Royal Swedish Academy of Sciences. He also serves as Vice Chairman of the Board of Directors of the Nobel Foundation and has been a member of the Nobel Assembly at Karolinska Institute since 1997. He chaired its Nobel Committee 2004-6 and was its secretary and Director of the Medical Nobel Institute 2009-2014. He is a member of Academia Europaea and has received several awards and honorary doctorates for his contributions to medicine.

Dr Hansson´s research deals with immune and inflammatory mechanisms in atherosclerosis. He discovered that atherosclerosis involves a local inflammatory immune response in the artery wall, that low-density lipoprotein (LDL) can act as an autoantigen, and that immunosuppressive drugs inhibit arterial restenosis, a principle used in current therapy. His current work deals with T cell differentiation, immunoregulatory mechanisms, and atheroprotective immunity.

Dr Hansson has published 410 scientific papers (including original papers, reviews, and chapters), supervised 24 PhD students and 18 postdoctoral fellows.


Mon 24 Apr

Keynote Lecture: How LDL causes inflammation in the artery wall

Chair:
  • Jan Borén
  • Alberico L. Catapano

Dr Hansson´s research deals with immune and inflammatory mechanisms in atherosclerosis. He discovered that atherosclerosis involves a local inflammatory immune response in the artery wall, that low-density lipoprotein (LDL) can act as an autoantigen, and that immunosuppressive drugs inhibit arterial restenosis, a principle used in current therapy. His current work deals with T cell differentiation, immunoregulatory mechanisms, and atheroprotective immunity. In his Key Note Lecture, Dr Hansson will discuss: ‘How LDL causes inflammation in the artery wall.’

Atherosclerosis is a chronic inflammatory disease which is triggered by the retention and accumulation of cholesterol-containing lipoproteins, particularly LDL, in the artery wall. Modification of these lipoprotein components can trigger activation of the innate immune response. Apolipoprotein B-100 also contributes to vascular inflammation by triggering the response of T and B cells locally.

Pattern recognition receptors play a key role in these processes. Lipid overload in macrophages activates the inflammasome and initiates the innate immune response; Toll-like receptors recognize and bind modified lipoprotein particles in the arterial intima, triggering processes that lead to expression of pro-inflammatory genes; and dendritic cells from the lesion containing fragments of LDL particles drive the adaptive immunity response. Peptide fragments of apolipoprotein B can act as autoantigens, resulting in differentiation of T cells to pro-inflammatory Th1 effector cells. Furthermore, these T cells may undergo reactivation by LDL fragments, leading to progressive inflammation, which in turn influences the initiation, progression, and stability of atherosclerotic plaque.

As a consequence, the immune-inflammatory axis has become a key focus in the search for novel possibilities for preventing progression of atherosclerosis beyond lipid-lowering.