Article Text


SP0091 E-selectin deletion constructs allow the study of differential binding of mononuclear and polymorphonuclear leukocytes to e-selectin in inflammation
  1. R Hallmann1,
  2. A Krause1,
  3. M Laschinger2,
  4. B Engelhardt2,
  5. RO Hynes3,
  6. M Hammel1
  1. 1Experimental Medicine I, University Erlangen-Nuernberg, Erlangen
  2. 2Molecular Cell Biology, Max-Planck-Institute, Bad Nauheim, Germany
  3. 3Pathology, Harvard Medical School, Harvard, USA


Endothelial cell activation is an important step in the inflammatory cascade which leads to the extravasation of leukocytes into the site of inflammation. The rolling of leukocytes is the beginning of this cascade and is mediated by the selectins. We have analysed the binding of both polymorphonuclear granulocytes and mononuclear cells to E-selectin presented exclusively by activated vascular endothelial cells. Four different monoclonal antibodies inhibited this adhesion differentially, and deletion constructs of E-selectin expressed on endothelial cells were also functionally distinguishable by their interaction with granulocytes and lymphocytes, respectively. Different binding mechanisms for these leukocyte subsets to endothelial E-selectin are proposed and signalling mechanisms via E-selectin, in particular Ca2+ signals into the leukocyte will be discussed.

Statistics from

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.