Prof. Dr. Esther Lutgens

Profil

FachgebietPathologie
KeywordsAtherosclerosis, Immune System, Inflammation

Aktuelle Kontaktadresse

LandDeutschland
OrtMünchen
Universität/InstitutionLudwig-Maximilians-Universität München (LMU)
Institut/AbteilungKlinikum der Universität München

Gastgeber*innen während der Förderung

Prof. Dr. Christian WeberInstitut für Molekulare Herz-Kreislauf-Forschung (IMCAR), Rheinisch-Westfälische Technische Hochschule Aachen (RWTH), Aachen
Prof. Dr. Christian WeberInstitut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten (August-Lenz-Stiftung), Ludwig-Maximilians-Universität München (LMU), München
Beginn der ersten Förderung01.12.2008

Programm(e)

2008Sofja Kovalevskaja-Preis-Programm

Projektbeschreibung der*des Nominierenden

Cardiovascular disease is responsible for almost half of the morbidity and mortality worldwide, causing an alarming 7 million cases of death in Europe and North America in 2006, and develops mostly from atherosclerosis and the resulting obstruction or thrombosis of large arteries. As evident by a prominent infiltration with immune cells, it is now widely accepted that atherosclerosis is a chronic inflammatory disease with a pivotal role for the innate and adaptive immune system. The co-stimulatory molecules CD40 and CD40L responsible for expansion and differentiation of naive T-lymphocytes into effecor-cells have been identified as key players in atherosclerotic plaque progression. Since the clinical complications of atherosclerosis mostly result from plaque rupture, induction of plaque stability will reduce the morbidity and mortality of atherosclerosis. Professor Lutgens hypothesizes that targeting recently identified atherosclerosis-specific components of the CD40-CD40L pathway, e.g. CD40-TRAF6, will be a valuable therapeutic strategy to induce stable plaques without immune-suppressive side-effects. The downstream pathways of CD40 and their therapeutic suitability will be elucidated in atherosclerotic mice, in which components of the CD40-pathway have been modified.