"For me, I couldn't imagine doing anything else. I love my work. It's fun, interesting and intellectually challenging every day, to think it through. It's real." - Klaus Ley, M.D.
Dr. Ley joined LIAI in 2007 as the Division Head in the Division of Inflammation Biology.
Dr. Ley received his B.S. from Altkönigschule-Gymnasium, Kronberg, Germany in 1976. In 1982, he received his M.D. from
the Julius-Maximilians-Universität, Würzburg, Germany. Dr. Ley began
his postdoctoral training from 1983 to 1987 at the Freie Universität Berlin, Germany. From 1987 to 1989, Dr. Ley was a visiting
research scientist at the University of California, San Diego. From
1990 to 1992, Dr. Ley was appointed as scientific assistant for the
Department of Physiology at Freie Universität in Berlin, Germany.
Dr. Ley has been awarded the 2008 Marie T. Bonazinga Award, the highest scientific prize offered by the Society for Leukocyte Biology, and the 2010 Malpighi Award, the most prestigious award of the European Society for Microcirculation.
Klaus Ley, M.D., and his team study inflammation a defense
reaction caused by tissue damage or injury, characterized by redness,
heat, swelling, and pain. The primary objective of inflammation is to
localize and eradicate the irritant and repair the surrounding tissue.
For the survival of the host, inflammation is a necessary and
beneficial process. The inflammatory response involves three major
stages: first, dilation of capillaries to increase blood flow; second,
microvascular structural changes and escape of plasma proteins from the
bloodstream; and third, leukocyte transmigration through endothelium
and accumulation at the site of injury.
The leukocyte adhesion cascade is a sequence of adhesion and
activation events that ends with extravasation of the leukocyte,
whereby the cell exerts its effects on the inflamed site. At least five
steps of the adhesion cascade are capture, rolling, slow rolling, firm
adhesion, and transmigration. Each of these five steps appears to be
necessary for effective leukocyte recruitment, because blocking any of
the five can severely reduce leukocyte accumulation in the tissue.
These steps are not phases of inflammation, but represent the sequence
of events from the perspective of each leukocyte. At any given moment,
capture, rolling, slow rolling, firm adhesion and transmigration all
happen in parallel, involving different leukocytes in the same
The roles of adhesion molecules in acute and chronic
inflammation have been investigated using in vitro model systems and in
vivo microcirculation studies. The ultimate goal of inflammation
research is to develop methods to control inflammation by modulating or
blocking leukocyte adhesion to the endothelium. These ideas developed
by basic research contribute to contemporary research projects
developing anti-inflammatory drugs. Anti-inflammatory agents function
as blockers, suppressors, or modulators of the inflammatory response.
Leukocyte ligands for endothelial selectins: specialized glycoconjugates that mediate rolling and signaling under flow. Blood. 2011
SAMP1/YitFc mouse strain: A spontaneous model of Chron's disease-like ileitis.
Inflamm Bowel Dis. 2011
How dendritic cells shape atherosclerosis. Trends Immunol. 2011
CD63 positions CD62P for rolling. Blood. 2011
High refractive index silicone gels for simultaneous total internal reflection flourescence and traction force microscopy of adherent cells. PLoS One. 2011
Small moleculemediated activation of the integrin CD11b/CD18 reduces inflammatory disease. Sci Signal. 2011
Monocyte and macrophage dynamics during atherogenesis. Arterioscler Thromb Vasc Biol. 2011
Rap1a activation by CalDAG-GEFI and p38 MAPK is involved in Eselectin-dependent slow leukocyte rolling. Eur J Immunol. 2011
Adam 17-dependent shedding limits early neutrophil influx but does not alter early monocyte recruitment to inflammatory sites. Blood. 2011
Live cell imaging of paxillin in rolling neutrophils by dual-color quantitative dynamic footprinting. Microcirculation. 2011
Protein tyrosine kinases in neutrophil activation and recruitment. Arch Biochem Biophys. 2011
Flow cytometry analysis of immune cells within murine aortas. J Vis Exp. 2011
Cell protrusions and tethers: a unified approach. Biophys J. 2011
Protein kinase C isoforms in neutrophil adhesion and activation. Arch Immunol Ther Exp. 2011
Mycophenolate mofetil decreases atherosclerotic lesion size by depression of aortic T lymphocyte and IL-17-mediated macrophage accumulation. J Am Coll Cardiol. 2011
Prevention, but not cure of type 1 diabetes by FTY720 in NOD/LtJ mice despite effective modulation of blood T cells. Autoimmunity. 2011
Biomechanics of leukocyte rolling. Biorheology. 2011
Development of monocytes, macrophages, and dendritic cells. Science. 2010
CXC chemokine ligand 4 induces a unique transcriptome in monocyte-derived macrophages. J Immunol. 2010
CXCL4 downregulates the atheroprotective hemoglobin receptor CD163 in human macrophages. Circ Res. 2010
ReSASC: a resampling-based algorithm to determine differential protein expression from spectral count data. Proteomics. 2010
View all publications
The link above may include papers by scientists with the same or similar name.
Click researcher's name for e-mail. Dial 858-752-6500 to call.