biography
"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 Scientific Award of the European
Society for Microcirculation (1986), the Medizinische
Grundlagenforschung from the Smith-Kline-Beechum Foundation (1992), the
Finalist award by the American Heart Association (1998), the Annual
Gelber Lecture Award from the Baylor College of Medicine (2000), and
the Kurt Anderson Lecturer award from the University of Texas,
Galveston (2001).
research focus
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
microvessels.
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.
selected publications
Cell adhesion under flow. Microcirculation. 2009
Immune and inflammatory mechanisms of atherosclerosis. Ann. Rev. Immunology. 2009
Transcriptional regulation of mouse L-Selectin. Biochim Biophys Acta. 2009
Event tracking model of adhesion identifies load-bearing bonds in rolling leukocytes. Microcirculation. 2009
Neutrophil adhesion and activation under flow. Microcirculation. 2009
Blockade of CD40L signaling attenuates leukocyte accumulation and neointima formation after carotid denudation injury in apolipoprotein E-deficient mice. Am.J.Pathol. 2008
Upregulation of aldose reductase during foam cell formation as possible link between diabetes, hyperlipidemia and atherosclerosis. ATVB. 2008
Monocyte-endothelial cell interactions in the development of atherosclerosis. Trends Cardiovasc Med. 2008.
Interleukin-17A inhibits the expansion of IL-17A-producing T cells in mice through "short-loop" inhibition via IL-17 receptor. J. of Immunology. 2008
Sialyltransferase ST3Gal-IV controls CXCR2-mediated firm leukocyte arrest during inflammation. J. Exp. Med. 2008
Therapeutic inhibition of CXCR2 by Reparixin attenuates acute lung injury (ALI) in mice. Br. J. Pharmacol. 2008
PECAM-1-dependent endothelial shear stress response promotes atherosclerotic lesions in areas of disturbed flow. ATVB. 2008
Platelet chemokines in vascular disease. ATVB. 2008
Endothelial Cell PECAM-1 Promotes Atherosclerotic Lesions in Areas of Disturbed Flow in ApoE-Deficient Mice. ATVB. 2008
PSGL-1 engagement by E-selectin signals through Src kinase Fgr and ITAM-adapters DAP12 and FcRγ to induce slow leukocyte rolling. J. Exp. Med. 2008
Mechanisms and consequences of neutrophil interaction with the endothelium. Biological Perspectives Series, Am. J. Pathol. 2008
Plasma-derived microparticles for biomarker discovery. Clinical Laboratory. 2008.
Cells on the run: shear-regulated integrin activation in leukocyte rolling and arrest on endothelial cells. Current Opinion in Cell Biology. 2008
Leukocyte adhesion molecules in animal models of inflammatory bowel disease. Inflammatory Bowel Diseases. 2008
Homeostatic regulation of blood neutrophil counts. J. Immunol. 2008
From lung injury to fibrosis. Nature Medicine. 2008
Dances with leukocytes: how tetraspanin-enriched microdomains assemble to form endothelial adhesive platforms. J.Cell Biol. 2008
View all publications
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