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Blood, 1 August 2006, Vol. 108, No. 3, pp. 928-935.
Prepublished online as a Blood First Edition Paper on April 13, 2006; DOI 10.1182/blood-2005-09-010629.
 Previous Article | Next Article 
Submitted September 23, 2005
Accepted March 21, 2006
Platelet-derived LIGHT induces inflammatory responses in
endothelial cells and monocytes
Kari Otterdal*, Camilla Smith, Erik Oie, Turid M Pedersen, Arne Yndestad, Espen Stang, Knut Endresen, Nils O Solum, Pal Aukrust, and Jan K Damas
Research Institute for Internal Medicine, Rikshospitalet University Hospitalet
Research Institute for Internal Medicine, Rikshospitalet University Hospitalet
Institute for Surgical Research and Department of Cardiology, Rikshospitalet University Hospitalet
Institute of Pathology, Rikshospitalet University Hospitalet
Department of Cardiology, Rikshospitalet University Hospitalet
Rikshospitalet University Hospitalet
Section of Clinical Immunology and Infectious Diseases, Rikshospitalet University Hospitalet
* Corresponding author; email: kari.otterdal{at}medisin.uio.no.
Traditionally, platelets are known to play an important
role in hemostasis, thrombosis and wound healing, but
increasing evidence suggests that activated platelets
also may promote inflammation. Platelet-induced
modulation of inflammation seems to involve platelet
expression of ligands in the tumor necrosis factor (TNF)
superfamily such as CD40 ligand and Fas ligand. The
present study demonstrates that LIGHT, another member of
the TNF superfamily, is associated with platelets and is
released as a soluble ligand upon platelet activation.
The release of LIGHT involves GP IIb/IIIa-dependent
mechanisms and action of metal-dependent proteases as
well as intracellular processes such as actin
polymerization. We also report that platelet-derived
LIGHT is biologically active, and can induce an
inflammatory response in monocytes and particularly
within endothelial cells measured as up-regulation of
adhesion molecules and release of chemokines. Moreover,
we demonstrate that thrombus material, obtained at the
site of plaque rupture in patients with acute myocardial
infarction, contains platelet-associated LIGHT,
suggesting that LIGHT-mediated inflammation also is
operating in vivo within an inflamed and thrombotic
vessel wall. The data may suggest a pathogenic role for
platelet-derived LIGHT in atherogenesis and plaque
destabilization as well as in other inflammatory
disorders involving leukocyte infiltration into the
vessel wall.
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