Project Details
Projekt
Pro-inflammatory interleukin-17A: a modulator of atherogenesis
Applicant
Dr. Christian Erbel
Subject Area
Cardiology, Angiology
Term
from 2013 to 2015
Project identifier
Deutsche Forschungsgemeinschaft (DFG) - Project number 231955177
Atherosclerosis and its complications such as myocardial infarction and stroke are one of the main causes of death in industrialized nations. Atherogenesis is based on a chronic inflammatory process, involving the immunocompetent cells such as T cells, macrophages and dendritic cells. The inflammatory milieu in the lesions, which e.g. seem to affect the polarization of macrophages, is also influenced by tertiary lymphoid structures located in the adventitia of the aorta. Preliminary work in our group show that the inhibition of pro-inflammatory cytokine interleukin-17A (IL-17A) in apolipoprotein E deficient mice significantly reduced the formation of atherosclerotic lesions. Possible mechanisms are a reduction in plaque inflammation and recruitment of inflammatory cells into the lesion. Our hypothesis is that IL-17A plays a crucial role as a modulator of the development, the progress and vulnerability of atherosclerosis. We intend to examine this hypothesis through the following approaches: (1) Effect of IL-17A inhibition on already established atherosclerotic lesions. (2) Influence of IL-17A on the differentiation and polarization of macrophages. (3) Role of IL-17A on tertiary lymphoid structures in the aortic adventitia.
DFG Programme
Research Grants
International Connection
USA
