Apoptotic-cell-derived membrane microparticles and IFN-α induce an inflammatory immune response

• Verfasst von: Nießen, Anna [VerfasserIn]
• Verfasst von: Heyder, Petra [VerfasserIn]
• Verfasst von: Krienke, Stefan [VerfasserIn]
• Verfasst von: Blank, Norbert [VerfasserIn]
• Verfasst von: Tykocinski, Lars-Oliver [VerfasserIn]
• Verfasst von: Lorenz, Hanns-Martin [VerfasserIn]
• Verfasst von: Schiller, Martin [VerfasserIn]
• Titel: Apoptotic-cell-derived membrane microparticles and IFN-α induce an inflammatory immune response
• Verf.angabe: Anna Niessen, Petra Heyder, Stefan Krienke, Norbert Blank, Lars-Oliver Tykocinski, Hanns-Martin Lorenz, Martin Schiller
• E-Jahr: 2015
• Jahr: 15 July 2015
• Umfang: 11 S.
• Fussnoten: Gesehen am 23.02.2017
• Titel Quelle: Enthalten in: Journal of cell science
• Ort Quelle: Cambridge : Company of Biologists Limited, 1853
• Jahr Quelle: 2015
• Band/Heft Quelle: 128(2015), 14, Seite 2443-2453
• ISSN Quelle: 1477-9137
• DOI: doi:10.1242/jcs.162735
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1553758501

Abstract

A Section a dysregulation in the clearance of apoptotic material is considered a major pathogenetic factor for the emergence of autoimmune diseases. Apoptotic-cell-derived membrane microparticles (AdMPs), which are released from the cell surface during apoptosis, have been implicated in the pathogenesis of autoimmunity. Also of importance are cytokines, such as interferon-α (IFN-α), which is known to be a major player in patients with systemic lupus erythematosus (SLE). This study investigates the combined effect of AdMPs and IFN-α on professional phagocytes. In the presence of IFN-α, phagocytosis of AdMPs by human monocytes was significantly increased in a dose-dependent manner. The combination of AdMPs and raised IFN-α concentrations resulted in an increase in the secretion of pro-inflammatory cytokines and an upregulation of surface molecule expression involved in antigen uptake. In addition, macrophage polarisation was shifted towards a more inflammatory type of cell. The synergism between IFN-α and AdMPs seemed to be mediated by an upregulation of phosphorylated STAT1. Our results indicate that IFN-α, together with AdMPs, amplify the initiation and maintenance of inflammation. This mechanism might especially play a crucial role in disorders with a defective clearance of apoptotic material.