"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).

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.

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

PSGL-1-dependent myeloid leukocyte activation. J Leukoc Biol. 2009

Role of beta7 integrins in intestinal lymphocyte homing and retention. Curr Mol Med. 2009 

Glycosylation in immune cell trafficking. Immunol Rev. 2009 

Immune and inflammatory mechanisms of atherosclerosis. Ann. Rev. Immunology. 2009 

T-lineage cells require the thymus but not VDJ recombination to produce IL-17A and regulate granulopoiesis in vivo. J Immunol. 2009

Dynamics of Microvillus Extension and Tether Formation in Rolling Leukocytes. Cell Mol Bioeng. 2009

Homeostatic regulation of blood neutrophil counts. J Immunol. 2008

PSGL-1 engagement by E-selectin signals through Src kinase Fgr and ITAM adapters DAP12 and FcR gamma to induce slow leukocyte rolling. J Exp Med. 2008 

Spleen tyrosine kinase Syk is necessary for E-selectin-induced alpha(L)beta(2) integrin-mediated rolling on intercellular adhesion molecule-1. Immunity. 2007 

Complete reversal of acid-induced acute lung injury by blocking of platelet-neutrophil aggregation. J Clin Invest. 2006 

Critical role of endothelial CXCR2 in LPS-induced neutrophil migration into the lung. J Clin Invest. 2006

Circulating activated platelets exacerbate atherosclerosis in mice deficient in apolipoprotein E.
Nat Med. 2003 

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