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Maria Orietta Borghi

Researcher at University of Milan

Publications -  160
Citations -  5029

Maria Orietta Borghi is an academic researcher from University of Milan. The author has contributed to research in topics: Antiphospholipid syndrome & Antibody. The author has an hindex of 40, co-authored 151 publications receiving 4386 citations.

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Role of the MyD88 transduction signaling pathway in endothelial activation by antiphospholipid antibodies

TL;DR: It is demonstrated that anti-beta(2)-GPI antibodies react with their antigen likely associated to a member of the TLR/IL-1 receptor family on the EC surface and directly induce activation, suggesting an involvement of the toll-like receptor (TLR) family.
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Antiphospholipid antibodies and the antiphospholipid syndrome: pathogenic mechanisms.

TL;DR: This article addresses molecular events triggered by aPL Abs on endothelial cells, platelets, and monocytes and complement activation, as well as a review of the current knowledge with regard to the putative receptor(s) recognized by a PL Abs on target cells aswell as novel mechanisms that involve fibrinolytic processes.
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Toll‐like receptor and antiphospholipid mediated thrombosis: in vivo studies

TL;DR: Findings in LPS−/− mice and the reduction in the “protective” polymorphism in patients with APS with thrombosis suggest that TLR-4 is involved in the interaction of aPL with endothelial cells in vivo.
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Relationship between anti-phospholipid and anti-endothelial cell antibodies III: beta 2 glycoprotein I mediates the antibody binding to endothelial membranes and induces the expression of adhesion molecules.

TL;DR: Findings indicate that the close association between anti-endothelial and anti-phospholipid antibodies is sustained by antibodies which recognize beta 2 GPI adhering to the endothelial cells, and can promote their activation.
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TH1 and TH2 cytokine production by peripheral blood mononuclear cells from HIV-infected patients

TL;DR: In the course of HIV disease mitogen-stimulated IL-2 production decreased, spontaneous and stimulated IL-6 production and spontaneous IL-10 secretion increased, and a switch from a type 1 to a type 2 response occurs in HIV infection.