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“You don't cure the disease by only looking at the disease.
 Very often cures come out of left field. ”
Klaus Ley, M.D.
Head and Member
Autoimmune Research; Inflammation Biology
Contact
biography

cell-bullet1.jpg"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

cell-bullet2.jpg 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-bullet3.jpg 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
The link above may include papers by scientists with the same or similar name.

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AWARDS AND HONORS
  • Biomedical Engineering Society, Fellow, 2005
  • Plenary Lecturer at the annual ATVB Conference, 2005
  • Faculty of 1000, elected contributing member of Cell Biology section, 2003
  • Kurt Anderson Memorial Lectureship, UTMB Galveston, 2001
  • Curt A. Wiederhielm Award of the Microcirculatory Society, 2001
  • American Institute for Medical and Biological Engineering (AIMBE), Elected Fellow, 2001
  • Annual Gelber Lecturer, Baylor College of Medicine, 2000
  • NIH Pathology A study section, charter member, 2000-2004
  • Finalist, American Heart Association Basic Science Prize, 1998 
  • Basic Medical Research Award (Medizinische Grundlagenforschung), Smith-Kline-Beecham Foundation, 1992
  • Abbott Award: Scientific award of the European Society for Microcirculation, 1986
  • M.D. Research Thesis, summa cum laude, 1983
  • Pre-doctoral research fellowship by Studienstiftung des Deutschen Volkes, 1980
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