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Blood, 1 August 2007, Vol. 110, No. 3, pp. 1029-1035.
Prepublished online as a Blood First Edition Paper on April 23, 2007; DOI 10.1182/blood-2007-01-069195.
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Submitted January 23, 2007
Accepted April 19, 2007
TREM-1 ligand expression on platelets enhances neutrophil activation
Philipp Haselmayer, Ludger Grosse-Hovest, Philipp von Landenberg, Hansjorg Schild, and Markus Philipp Radsak*
Institute for Immunlogy, University of Mainz, Mainz, Germany
Department of Immunology, Institute for Cell Biology, University of Tubingen, Tubingen, Germany
Department of Clinical Chemistry, University Hospital, Johannes Gutenberg-University, Mainz, Germany
IIIrd Department of Medicine, University Hospital, Johannes Gutenberg-University, Mainz, Germany
* Corresponding author; email: radsak{at}uni-mainz.de.
The triggering receptor expressed on myeloid cells (TREM) 1 plays an important role in the innate immune response related to severe infections and sepsis. Modulation of TREM-1 associated activation improves the outcome in rodent models for pneumonia and sepsis. However, the identity and occurrence of the natural TREM-1 ligands are so far unkown impairing the further understanding of the biology of this receptor. Here, we report the presence of a ligand for TREM-1 on human platelets. Using a recombinant TREM-1 fusion protein we demonstrate specific binding of TREM-1 to platelets. TREM-1 specific signals are required for the platelet induced augmentation of PMN effector functions (provoked by LPS). However TREM-1 interaction with its ligand is not required for platelet/PMN complex formation which is dependent on integrins and selectins. Taken together, the TREM-1 ligand is expressed by platelets and the TREM-1/ligand interaction contributes to the amplification of LPS induced PMN activation. Our results shed a new light on our understanding of TREM-1 and its role in the innate inflammatory response in infections and might contribute to the development of future concepts to treat sepsis.
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