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Brief Communication
Nature Medicine 11, 1167 - 1169 (2005)
Published online: 30 October 2005; | doi:10.1038/nm1317

Platelets mediate cytotoxic T lymphocyte–induced liver damage

Matteo Iannacone1, 2, Giovanni Sitia2, Masanori Isogawa1, Patrizia Marchese1, Maria G Castro3, 4, Pedro R Lowenstein3, 4, Francis V Chisari1, Zaverio M Ruggeri1 & Luca G Guidotti1, 2

1  Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA.

2  Immunopathogenesis of Liver Infections Unit, San Raffaele Scientific Institute, Via Olgettina 58, Milan, 20132 Italy.

3  Board of Governors Gene Therapeutics Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048, USA.

4  Department of Molecular and Medical Pharmacology, University of California at Los Angeles, Box 951735, 23-138 CHS, Los Angeles, California 90095, USA.

Correspondence should be addressed to Luca G Guidotti guidotti@scripps.edu

We found that platelet depletion reduces intrahepatic accumulation of virus-specific cytotoxic T lymphocytes (CTLs) and organ damage in mouse models of acute viral hepatitis. Transfusion of normal but not activation-blocked platelets in platelet-depleted mice restored accumulation of CTLs and severity of disease. In contrast, anticoagulant treatment that prevented intrahepatic fibrin deposition without reducing platelet counts did not avert liver injury. Thus, activated platelets contribute to CTL-mediated liver immunopathology independently of procoagulant function.


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ISSN: 1078-8956
EISSN: 1546-170X
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