CD95L mediates tumor counterattack in vitro but induces neutrophil-independent tumor rejection in vivo

• Verfasst von: Igney, Frederik [VerfasserIn]
• Verfasst von: Behrens, Christian [VerfasserIn]
• Verfasst von: Krammer, Peter H. [VerfasserIn]
• Titel: CD95L mediates tumor counterattack in vitro but induces neutrophil-independent tumor rejection in vivo
• Verf.angabe: Frederik H. Igney, Christian K. Behrens and Peter H. Krammer
• Jahr: 2005
• Jahr des Originals: 2004
• Umfang: 10 S.
• Teil: volume:113
• Teil: year:2005
• Teil: number:1
• Teil: pages:78-87
• Teil: extent:10
• Fussnoten: First published: 25 August 2004 ; Gesehen am 04.03.2021
• Titel Quelle: Enthalten in: International journal of cancer
• Ort Quelle: Bognor Regis : Wiley-Liss, 1966
• Jahr Quelle: 2005
• Band/Heft Quelle: 113(2005), 1, Seite 78-87
• ISSN Quelle: 1097-0215
• DOI: doi:10.1002/ijc.20538
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: apoptosis
• Sach-SW: CTL
• Sach-SW: immune escape
• Sach-SW: neutrophils
• K10plus-PPN: 1750397501

Abstract

Many tumors express CD95L (CD178, FasL, APO-1L) and may thus kill tumor-infiltrating lymphocytes, a phenomenon called tumor counterattack. However, presently it is not clear whether tumor counterattack is a relevant immune escape mechanism. To characterize the effect of CD95L expression of tumor cells on tumor-specific T cells, we established an in vitro system with TCR tg T cells and a model tumor antigen. Preactivated antitumor T cells were able to kill CD95L− and CD95L+ tumor cells. CD95L+ tumor cells killed activated T cells in vitro and inhibited the expansion of cytotoxic antitumor T cells in mixed lymphocyte tumor reactions. In vivo CD95L expression led to delayed tumor growth or complete tumor rejection. Neutrophils were not responsible for the delayed growth of the CD95L+ tumors tested. In mice with neutrophils deficient for important cytotoxicity mechanisms (p47phox−/− or iNOS−/− mice), CD95L+ tumors grew similarly as in wild-type mice. Incidence and growth rate of CD95L+ tumors in mice injected with a neutrophil-depleting or an isotype control antibody was the same. In CD95-deficient lpr mice, tumor growth was not altered as compared to wild-type mice. Taken together, CD95L mediated tumor counterattack in vitro, but led to neutrophil-independent tumor rejection in vivo.