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Antonella Capozzi

Researcher at Sapienza University of Rome

Publications -  60
Citations -  1245

Antonella Capozzi is an academic researcher from Sapienza University of Rome. The author has contributed to research in topics: Antiphospholipid syndrome & Lipid raft. The author has an hindex of 16, co-authored 51 publications receiving 959 citations.

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Autoantibodies specific to a peptide of β2-glycoprotein I cross-react with TLR4, inducing a proinflammatory phenotype in endothelial cells and monocytes

TL;DR: A novel pathogenic mechanism in the TLR4 stimulation by anti-β(2)GPI peptide Abs that links adaptive immune responses with innate immunity in antiphospholipid syndrome and systemic lupus erythematosus is suggested.
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The Mosaic of “Seronegative” Antiphospholipid Syndrome

TL;DR: Findings suggest that in sera from patients with SN-APS, antibodies may be detected using “new” antigenic targets (mainly vimentin/cardiolipin) or methodological approaches different from traditional techniques (Mainly TLC immunostaining).
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Subclinical atherosclerosis in systemic lupus erythematosus and antiphospholipid syndrome: focus on β2GPI-specific T cell response

TL;DR: A significant percentage of patients with SLE and PAPS show a &bgr;2GPI-specific T cell reactivity, which is associated with subclinical atherosclerosis, and this work confirms a link between autoimmunity and endothelial dysfunction.
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New antigenic targets and methodological approaches for refining laboratory diagnosis of antiphospholipid syndrome

TL;DR: Recent findings suggest that, in sera from patients with SN-APS, antibodies may be detected using “new” antigenic targets (mainly vimentin/cardiolipin) or methodological approaches different from traditional techniques (TLC immunostaining).
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Autoantibodies to the adenosine triphosphate synthase play a pathogenetic role in Alzheimer's disease.

TL;DR: Findings suggest that autoantibodies specific to ATP synthase can exert a pathogenetic role via a mechanism that brings into play the impairment of the extracellular ATP homeostasis and the alteration of mitochondrial function triggering cell death by apoptosis.