Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6119229 | Journal of Autoimmunity | 2014 | 9 Pages |
Abstract
Our findings demonstrate that β2GPI interacts directly with TLR4 expressed on EC, and that such interaction may contribute to β2GPI-dependent aPL-mediated EC activation. At variance of monocytic cells, we also showed a threshold effect for the action of LPS, that is able to enhance anti-β2GPI antibody EC binding only at cell activating concentrations, shown to increase TLR4 expression. This in vitro model may explain why LPS behaves as a second hit increasing the expression of β2GPI in vascular tissues and triggering aPL-mediated thrombosis in experimental animals.
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Authors
Elena Raschi, Cecilia B. Chighizola, Claudia Grossi, Nicoletta Ronda, Rita Gatti, Pier Luigi Meroni, M. Orietta Borghi,