Tumor counterattack

• Verfasst von: Igney, Frederik [VerfasserIn]
• Verfasst von: Krammer, Peter H. [VerfasserIn]
• Titel: Tumor counterattack
• Titelzusatz: fact or fiction?
• Verf.angabe: Frederik H. Igney, Peter H. Krammer
• E-Jahr: 2005
• Jahr: 12 May 2005
• Umfang: 10 S.
• Teil: volume:54
• Teil: year:2005
• Teil: number:11
• Teil: pages:1127-1136
• Teil: extent:10
• Fussnoten: This article is a symposium paper from the conference ‘‘Tumor Escape and Its Determinants’’, held in Salzburg, Austria, on 10–13 October 2004 ; Gesehen am 02.03.2021
• Titel Quelle: Enthalten in: Cancer immunology immunotherapy
• Ort Quelle: Berlin : Springer, 1976
• Jahr Quelle: 2005
• Band/Heft Quelle: 54(2005), 11, Seite 1127-1136
• ISSN Quelle: 1432-0851
• DOI: doi:10.1007/s00262-005-0680-7
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1750132885

Abstract

Cancer development relies on a variety of mechanisms that facilitate tumor growth despite the presence of a functioning immune system. Understanding these mechanisms may foster novel therapeutic approaches for oncology and organ transplantation. By expression of the apoptosis-inducing protein CD95L (FasL, APO-1L, CD178), tumors may eliminate tumor-infiltrating lymphocytes and suppress anti-tumor immune responses, a phenomenon called “tumor counterattack”. On the one hand, preliminary evidence of tumor counterattack in human tumors exists, and CD95L expression can prevent T-cell responses in vitro. On the other hand, CD95L-expressing tumors are rapidly rejected and induce inflammation in mice. Here, we summarize and discuss the consequences of CD95L expression of tumor cells and its contribution to immune escape.