title: Tumor counterattack: fact or fiction?
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.
authors.affiliation: Tumor Immunology Program, German Cancer Research Center (DKFZ), Heidelberg, Germany. frederik.igney@schering.de
authors.forename: Frederik H
authors.initials: FH
authors.lastname: Igney
authors.forename: Peter H
authors.initials: PH
authors.lastname: Krammer
mesh_terms: D017209:Apoptosis; D053222:Fas Ligand Protein; D006801:Humans; D007249:Inflammation / Q000209:etiology; D008562:Membrane Glycoproteins / Q000032:analysis / Q000502:physiology*; D009369:Neoplasms / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D019139:Tumor Escape / Q000276:immunology*; D019014:fas Receptor / Q000502:physiology
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor