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P Rovere-Querini

Publications and source records attributed to P Rovere-Querini.

4 recordsLinked to original sources
PubMed2004

Accumulation of plasma nucleosomes upon treatment with anti-tumour necrosis factor-alpha antibodies.

OBJECTIVE: Patients undergoing anti-tumour necrosis factor-alpha (TNF-alpha) treatment often develop autoantibodies. Apoptotic cell antigens are a potential initiating stimulus for autoantibodies. Our goal was to verify whether anti-cytokine therapy causes the release of nucleosomes, a major autoantigen generated during cell death. DESIGN: Laboratory research study with comparison group. SETTING: Clinical Immunology Unit and Lab, H San Raffaele University Hospital, Italy. SUBJECTS: Eleven healthy controls and 87 rheumatic patients were studied, including 51 with rheumatoid arthritis (RA) and 33 patients with systemic lupus erythematosus (SLE). INTERVENTIONS: Vein blood samples were taken via the antecubital vein. Blood was retrieved from 11 patients before and after injection of anti-TNF-alpha humanized antibodies. Nucleosomes were measured with an enzyme-linked immunosorbent assay. Cell death induced by anti-TNF-alpha antibodies and by the soluble cytokine was assessed in vitro. MAIN OUTCOME MEASURES: Nucleosome level by treatment. RESULTS: Enzyme-linked immunosorbent assay effectively detected nucleosomes either released by dying cells in vitro or circulating in the plasma. SLE but not RA patients had circulating nucleosomes at the steady state. Eight of 11 patients had significantly higher levels of plasma nucleosomes after infliximab. Minute amounts of TNF-alpha enabled infliximab to induce cell death in vitro. CONCLUSIONS: The accumulation of nucleosomes possibly fosters the development of autoantibodies in subjects with appropriate genetic backgrounds.

Adolescent↗
PubMed2003

Corpse disposal after apoptosis.

The termination of the apoptotic program occurs in most cases via recognition and clearance by phagocytes. Engulfed cells do not simply disappear from the midst of living tissues. Constituents of the corpse indeed survive the intracellular processing and are recycled to the membrane of the phagocyte. The presentation of yielded antigens to T cells is a central event in the induction and the maintenance of peripheral tolerance. Conversely, errors in this pathway contribute to the pathogenesis of systemic and organ specific autoimmune diseases. Here we discuss the available information on the events that follow active engulfment of dying cells, with attention to the events involved in vitro and in vivo in apoptotic cell processing. The outcome of the processing is the cross-priming or the functional inactivation of T cells that specifically recognise antigens contained in the cell corpse.

Animals↗
PubMed2002

The disposal of dying cells in living tissues.

Cells continuously die and disappear from the midst of living tissues. However, some of their constituents survive. DNA is horizontally transferred to phagocytic cells, and apoptotic cell antigens shape the immune repertoire. When massive apoptosis occurs, which overwhelms tissue scavenger cells, or when the function of phagocytes abates, dying cells escape clearance in vivo. Remnant dying cells come to phagocytes disguised: factors capable to envelop their membranes pervade the entire organism, or are generated in given tissues. Some are constitutively present, while other are generated during early or late phases of the inflammatory response, possibly to face the further burden of the dead inflammatory cells. This camouflage influences the disposal of the corpses: decoying molecules either bridge the corpse to the phagocyte or hide it. Furthermore, factors associated to the plasma membrane of the apoptotic cell shape the signals the phagocyte releases in situ. Finally, molecules contained or released by the dying cell alter the apprehension by the phagocyte of its prey, influencing its immunogenicity.

Animals↗