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Blood, 15 February 2007, Vol. 109, No. 4, pp. 1507-1514. Prepublished online as a Blood First Edition Paper on November 2, 2006; DOI 10.1182/blood-2005-03-024463. This Article Full Text (PDF) Supplemental Table All Versions of this Article: blood-2005-03-024463v1 109/4/1507    most recent Alert me when this article is cited Alert me if a correction is posted 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 Satta, N. Articles by de Moerloose, P. Search for Related Content PubMed PubMed Citation Articles by Satta, N. Articles by de Moerloose, P. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted March 18, 2005 Accepted September 25, 2006 The role of TLR2 in the inflammatory activation of mouse fibroblasts by human antiphospholipid antibodies Nathalie Satta, Sylvie Dunoyer-Geindre, Guido Reber, Richard J Fish, Francoise Boehlen, Egbert KO Kruithof, and Philippe de Moerloose* Division of Angiology & Hemostasis, University Hospital, Faculty of Medicine, Geneva, Switzerland * Corresponding author; email: philippe.demoerloose{at}hcuge.ch. Antiphospholipid antibodies (APLA) promote inflammatory and procoagulant responses in endothelial cells and monocytes. Previous studies have shown that MyD88, TRAF6 and NF-B mediate cell activation by APLA. These intermediates are also employed by Toll-like receptors (TLR). We investigated the role of TLRs in the cellular response to APLA. IgG were isolated from the plasma of five antiphospholipid syndrome patients and immunopurified anti-2-glycoprotein 1 IgG from a sixth patient. Control IgG was obtained from a pool of healthy donor plasmas negative for APLA. Wild-type mouse embryonic fibroblasts (EF) and EF deficient in TLR1, TLR2, TLR4 or TLR6 were incubated with APLA, anti-2-glycoprotein 1 IgG or control IgG. Upon incubation with the patient IgG, but not control IgG, a significant increase in mRNA levels of the inflammatory marker proteins MCP-1, ICAM-1 and IL-6 as well as IL-6 secretion was observed in wild-type EF, whereas TLR2-deficient EF did not respond. Responses in TLR1- and TLR6-deficient EF were decreased and those in TLR4-deficient EF comparable to those in wild-type EF. Overexpression of human TLR2 in the TLR2-deficient EF restituted the response to patient IgG. Our results imply that TLR2 plays a role in mouse fibroblast activation by APLA. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E Raschi, M. Borghi, C Grossi, V Broggini, S Pierangeli, and P. Meroni Toll-like receptors: another player in the pathogenesis of the anti-phospholipid syndrome Lupus, October 1, 2008; 17(10): 938 - 943. [Abstract] [PDF]

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