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Blood, 15 January 2006, Vol. 107, No. 2, pp. 637-641. Prepublished online as a Blood First Edition Paper on September 22, 2005; DOI 10.1182/blood-2005-06-2202. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-06-2202v1 107/2/637    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Aslam, R. Articles by Semple, J. W. Search for Related Content PubMed PubMed Citation Articles by Aslam, R. Articles by Semple, J. W. Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Platelet Toll-like receptor expression modulates lipopolysaccharide-induced thrombocytopenia and tumor necrosis factor- production in vivo Rukhsana Aslam, Edwin R. Speck, Michael Kim, Andrew R. Crow, K. W. Annie Bang, Frederick P. Nestel, Heyu Ni, Alan H. Lazarus, John Freedman, and John W. Semple From the Department of Laboratory Medicine and Pathobiology, St Michael's Hospital, Toronto; the Departments of Pharmacology, Medicine, and Laboratory Medicine and Pathobiology, University of Toronto; Canadian Blood Services, Toronto; the Toronto Platelet Immunobiology Group, Toronto, ON; and the Faculty of Medicine, McGill University, Montreal, QC, Canada. Toll-like receptors (TLRs) play a critical role in stimulating innate immunity by recognizing pathogen-associated molecular patterns (PAMPs) on invading microorganisms. Platelets also play a role in innate immunity, and we studied whether they express TLR. Results show that human and murine platelets variably expressed TLR2, TLR4, and TLR9 by flow cytometry and Western blotting. TLR4 expression was confirmed by demonstrating murine platelet binding to lipopolysaccharide (LPS). Thrombin activation of the platelets significantly enhanced the expression of TLR9, suggesting that at least some TLRs may derive from intracellular compartments. When LPS was administered to LPS-sensitive C3H/HeN and LPS-resistant C3H/HeJ mice, functional TLR4 expression in vivo was shown to be responsible for LPS-induced thrombocytopenia. However, when the C3H/HeN mice were first rendered thrombocytopenic by an antiplatelet antibody and then administered LPS, a significant reduction occurred in their ability to produce TNF-. The decreased cytokine production in the thrombocytopenic mice was restored with platelet transfusion. These results suggest that platelets express various TLRs and that the functional significance of one of these, TLR4, appears to be a role in the modulation of LPS-induced thrombocytopenia and TNF- production. This work implicates platelets as important mediators of innate immune responses against invading microorganisms. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. Zhang, J. Han, E. J. Welch, R. D. Ye, T. A. Voyno-Yasenetskaya, A. B. Malik, X. Du, and Z. Li Lipopolysaccharide Stimulates Platelet Secretion and Potentiates Platelet Aggregation via TLR4/MyD88 and the cGMP-Dependent Protein Kinase Pathway J. 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