Fas (APO-1/CD95) in inflammatory CNS diseases

• Verfasst von: Faßbender, Klaus [VerfasserIn]
• Verfasst von: Eschenfelder, Christoph C. [VerfasserIn]
• Verfasst von: Hennerici, Michael G. [VerfasserIn]
• Titel: Fas (APO-1/CD95) in inflammatory CNS diseases
• Titelzusatz: intrathecal release in bacterial meningitis
• Verf.angabe: K. Fassbender, C. Eschenfelder, M. Hennerici
• E-Jahr: 1999
• Jahr: 11 January 1999
• Umfang: 4 S.
• Fussnoten: Gesehen am 27.07.2022
• Titel Quelle: Enthalten in: Journal of neuroimmunology
• Ort Quelle: Amsterdam [u.a.] : Elsevier Science, 1981
• Jahr Quelle: 1999
• Band/Heft Quelle: 93(1999), 1-2, Seite 122-125
• ISSN Quelle: 1872-8421
• DOI: doi:10.1016/s0165-5728(98)00210-0
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Adolescent
• Sach-SW: Adult
• Sach-SW: Aged
• Sach-SW: Aged, 80 and over
• Sach-SW: Apoptosis
• Sach-SW: Autoantigens
• Sach-SW: Blood-Brain Barrier
• Sach-SW: Cerebrospinal Fluid
• Sach-SW: fas Receptor
• Sach-SW: Female
• Sach-SW: Granulocytes
• Sach-SW: Humans
• Sach-SW: Male
• Sach-SW: Meningitis, Bacterial
• Sach-SW: Middle Aged
• Sach-SW: Solubility
• K10plus-PPN: 1811812996

Abstract

Release of Fas (APO-1, CD95), a type L-membrane protein which plays a crucial role in cytokine-mediated apoptosis was investigated in bacterial meningitis, viral meningoencephalitis and multiple sclerosis in vivo. After correction for bloodbrain-CSF-disruption, significantly increased intrathecal release of Fas was demonstrated exclusively in bacterial meningitis arguing for an apoptotic cell death of granulocytes in the subarachnoidal space aimed to self-limit inflammatory host response.