Antonella Capozzi

Pubblicazioni

Titolo Pubblicato in Anno
Effect of Heparanase inhibitor on Tissue Factor overexpression in platelets and endothelial cells induced by anti-β2-GPI antibodies JOURNAL OF THROMBOSIS AND HAEMOSTASIS 2021
Anti-vimentin/cardiolipin IgA in the antiphospholipid syndrome: a new tool for “seronegative” diagnosis CLINICAL AND EXPERIMENTAL IMMUNOLOGY 2021
Role of erlins in the control of cell fate through lipid rafts CELLS 2021
Overexpression of neuroglobin promotes energy metabolism and autophagy induction in human neuroblastoma SH-SY5Y cells CELLS 2021
Anti-Inflammatory Activity of a CB2 Selective Cannabinoid Receptor Agonist: Signaling and Cytokines Release in Blood Mononuclear Cells MOLECULES 2021
“Non-criteria antiphospholipid antibodies”: bridging the gap between seropositive and seronegative Antiphospholipid Syndrome RHEUMATOLOGY 2021
LRP6 mediated signal transduction pathway triggered by tissue plasminogen activator acts through lipid rafts in neuroblastoma cells JOURNAL OF CELL COMMUNICATION AND SIGNALING 2020
A multimolecular signaling complex including PrPC and LRP1 is strictly dependent on lipid rafts and is essential for the function of tissue plasminogen activator JOURNAL OF NEUROCHEMISTRY 2020
Raft-like lipid microdomains drive autophagy initiation via AMBRA1-ERLIN1 molecular association within MAMs AUTOPHAGY 2020
Molecular mechanisms of “antiphospholipid antibodies” and their paradoxical role in the pathogenesis of “seronegative APS” INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 2020
Tissue factor over-expression in platelets of patients with anti-phospholipid syndrome: induction role of anti-β2-GPI antibodies CLINICAL AND EXPERIMENTAL IMMUNOLOGY 2019
Reduction of autophagy and increase in apoptosis correlates with a favorable clinical outcome in patients with rheumatoid arthritis treated with anti-TNF drugs ARTHRITIS RESEARCH & THERAPY 2019
Alarmin HMGB1 and soluble RAGE as new tools to evaluate the risk stratification in patients with the antiphospholipid syndrome FRONTIERS IN IMMUNOLOGY 2019
Post-translational modifications of proteins in antiphospholipid antibody syndrome CRITICAL REVIEWS IN CLINICAL LABORATORY SCIENCES 2019
Neuroglobin overexpression plays a pivotal role in neuroprotection through mitochondrial raft-like microdomains in neuroblastoma SK-N-BE2 cells MOLECULAR AND CELLULAR NEUROSCIENCES 2018
A monocentric cohort of obstetric seronegative anti-phospholipid syndrome FRONTIERS IN IMMUNOLOGY 2018
Autophagy induces protein carbamylation in fibroblast-like synoviocytes from patients with rheumatoid arthritis RHEUMATOLOGY 2018
Anti-proliferative properties and proapoptotic function of new CB2 selective cannabinoid receptor agonist in jurkat leukemia cells INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 2018
Oxidative Stress Induces HSP90 Upregulation on the Surface of Primary Human Endothelial Cells: Role of the Antioxidant 7,8-Dihydroxy-4-methylcoumarin in Preventing HSP90 Exposure to the Immune System OXIDATIVE MEDICINE AND CELLULAR LONGEVITY 2018
Anti-mutated citrullinated vimentin antibodies in antiphospholipid syndrome: diagnostic value and relationship with clinical features IMMUNOLOGIC RESEARCH 2017

ERC

  • LS1
  • LS1_1
  • LS1_2
  • LS1_9

KET

  • Life-science technologies & biotechnologies

Interessi di ricerca

NUOVE SPECIFICITÀ ANTIGENICHE E NUOVE TECNOLOGIE NELLA DIAGNOSI DELLA SINDROME DA ANTICORPI ANTIFOSFOLIPIDI
L’identificazione di nuovi “targets” antigenici (es. cardiolipina/vimentina) e l’utilizzo di nuove metodologie, quali il TLC immunostaining e la chemiluminescenza, hanno permesso di perfezionare i test “anti-fosfolipidi”, consentendo sia una diagnosi differenziale fra pazienti con malattie autoimmuni e malattie infettive, sia l’identificazione di quei soggetti che risultano negativi ai test standard di laboratorio (pazienti sieronegativi). Nell’ambito degli studi volti a chiarire quali meccanismi siano alla base della comparsa degli anticorpi "anti-fosfolipidi” nelle malattie autoimmuni, molto importante è risultato il ruolo dell’apoptosi cellulare. Gli anticorpi anti-2-GPI (principale marker sierologico della Sindrome) possono riconoscere forme ossidate o glicate della proteina, inducendo la maturazione delle cellule dendritiche e promuovendo risposte di tipo Th1. Gli anticorpi possono innescare una via di trasduzione del segnale nelle cellule monocitarie, che porta al coinvolgimento dei recettori tipo TOLL, all’attivazione di fattori NF-kB, con conseguente produzione di citochine proinfiammatorie e fattori procoagulanti. L’insieme di questi studi ha permesso di comprendere le specificità antigeniche e le vie di trasduzione del segnale innescate dagli “anticorpi anti-fosfolipidi” nelle malattie autoimmunitarie, chiarendone il meccanismo patogenetico.

Keywords

autoimmune desease
antiphospholipid antibody syndrome
new technologies
diagnosis

© Università degli Studi di Roma "La Sapienza" - Piazzale Aldo Moro 5, 00185 Roma